<?xml version="1.0" encoding="utf-8"?>
<journal>
<language>en</language>
<journal_id_issn></journal_id_issn>
<journal_id_issn_online></journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi></journal_id_doi>
<journal_id_isnet></journal_id_isnet>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid></journal_id_sid>
<pubdate>
	<type>jalali</type>
	<year>1401</year>
	<month>1</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2022</year>
	<month>4</month>
	<day>1</day>
</pubdate>
<volume>26</volume>
<number>1</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Anticonvulsant effects of squill oxymel (a traditional formulation) in mice</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: This study evaluated the anticonvulsant activity of the add-on Drimia maritima (squill) oxymel, used traditionally in the treatment of convulsion, in animal model. Methods: Albino mice pretreated with squill oxymel in different doses of 50, 100, 200 and 400mg/kg by oral gavage, 15min prior to injection of pentylenetetrazole (PTZ). Animals pretreated with flumazenil to determine the mechanism of anticonvulsant action. The total flavonoid content of squill oxymel was also determined. Results: Squill oxymel prolonged the onset of seizures and decreased the duration of seizures compared to control group. Diazepam used as a reference drug for its anticonvulsive effects, showed complete inhibition of seizure. This study revealed that squill oxymel has significant anticonvulsant effect in PTZ-induced seizures in mice and these effects may be related to its effect on benzodiazepines&#8217; receptors on GABA complex. Conclusion: These results confirmed the traditional use of squill oxymel in Iranian traditional medicine for treatment of epilepsy. The clarification of mechanisms involved needs further studies.</abstract>
	<keyword_fa>Drimia maritime, Squill, Oxymel, Anticonvulsant, Pentylenetetrazole</keyword_fa>
	<keyword></keyword>
	<start_page>1</start_page>
	<end_page>6</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-15-1428-2&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/9
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/7/18
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1399/12/19
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Meysam</first_name>
	<middle_name></middle_name>
	<last_name>Abolmaali</last_name>
	<suffix></suffix>
	<affiliation>Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030953</code>
	<orcid>00319475328460030953</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Manijeh</first_name>
	<middle_name></middle_name>
	<last_name>Motevalian</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030954</code>
	<orcid>00319475328460030954</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Saeed</first_name>
	<middle_name></middle_name>
	<last_name>Mehrzadi</last_name>
	<suffix></suffix>
	<affiliation>Razi Drug Research Centre, Iran University of Medical Sciences, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030955</code>
	<orcid>00319475328460030955</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Asie</first_name>
	<middle_name></middle_name>
	<last_name>Shojaii</last_name>
	<suffix></suffix>
	<affiliation>Department of Traditional Pharmacy, School of Persian Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>shojaii.a@iums.ac.ir</email>
	<code>00319475328460030956</code>
	<orcid>00319475328460030956</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Enriched-asafoetida diet attenuates hyperglycemia, oxidative stress and endothelial dysfunction in type 2 diabetic rats</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: It has been documented that oxidative stress and inflammation are the main causes of diabetic-induced disorders. Several studies have been reported the antioxidant and antidiabetic effects of prepared asafoetida extracts, from Ferula assafoetida L. species in the Apiaceae family. The aim of the present study was to evaluate the effects of enriched-asafoetida diet (EAD) 0.5% and 2% on plasma level of glucose, hemoglobin A1C (HbA1C), insulin, lipid profile and hepatic enzymes, and vascular endothelial dysfunction induced by type 2 diabetes (T2D). Methods: Thirty-two male Wistar rats were divided into four groups: 1) control group, 2) diabetic group, 3 and 4) diabetic groups received EAD0.5% and EAD2% for 4 weeks, respectively. T2D was induced by intraperitoneal injection of nicotinamide and streptozotocin. At the end of the experiment, the plasma level of glucose, lipid profile, insulin, oxidative stress, hepatic enzymes and vascular dysfunction were evaluated. Results: Fasting blood sugar, HbA1C, oxidative stress and hepatic enzymes significantly decreased and plasma level of insulin markedly increased in the EAD0.5 compared to the diabetic group. The plasma lipid profile was improved in the EAD0.5 group. The response of thoracic aorta rings to vasodilators and vasoconstrictor substances was considerably improved in EAD0.5 than in the diabetic group. The EAD2 did not have a significant effect on diabetic induced disorders. Conclusion: The results of the present study suggest that the effects of EAD on biological disorders caused by T2D are dependent on the percentage of asafoetida in the diet.</abstract>
	<keyword_fa>Type 2 diabetes, Asafoetida, Hemoglobin A1C, Vascular dysfunction, Lipid profile.</keyword_fa>
	<keyword></keyword>
	<start_page>7</start_page>
	<end_page>19</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1525-1&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/23
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/11/4
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Mansour</first_name>
	<middle_name></middle_name>
	<last_name>Esmailidehaj</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>med1354@ssu.ac.ir</email>
	<code>00319475328460030679</code>
	<orcid>00319475328460030679</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mahboobe</first_name>
	<middle_name></middle_name>
	<last_name>Kahtenaroon</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030680</code>
	<orcid>00319475328460030680</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad Ebrahim</first_name>
	<middle_name></middle_name>
	<last_name>Rezvani</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030681</code>
	<orcid>00319475328460030681</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hossein</first_name>
	<middle_name></middle_name>
	<last_name>Azizian</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030682</code>
	<orcid>00319475328460030682</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Alimohammad</first_name>
	<middle_name></middle_name>
	<last_name>Ranjbar</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacognosy, School of Pharmacy Shahid Sadoughi University of Medical Sciences, Yazd, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030683</code>
	<orcid>00319475328460030683</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Naringin ameliorates cognitive impairment in streptozotocin/nicotinamide induced type 2 diabetes in Wistar rats</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Psychomotor slowing and reduced mental flexibility are symptoms of cognitive decline that can occur in type 2 diabetes disease (TD2). Strategies that combine the control of hyperglycaemia with prevention of cognitive decline are desirable. Thus, this study reports the effect of naringin on cognitive deficit in diabetic rats. Methods: TD2 in Wistar rats was induced with nicotinamide/streptozotocin (NA/STZ). Naringin (50 and 100 mg/kg) or glibenclamide (5mg/kg) was administered for 30 days to diabetic rats. Cognitive performance was investigated using the Morris water maze. Serum glucose, lipid profiles, brain tumour necrosis factor alpha (TNF-&#945;) and acetylcholinesterase (AChE) activity were determined. Results: Naringin and glibenclamide significantly reduced the escape latency, increased the time spent in the correct quadrant and number of entries in diabetic rats. Also, naringin reduced blood glucose, serum cholesterol, low-density lipoprotein cholesterol levels, triglycerides and prevented a decrease in the level of high-density lipoprotein cholesterol, in diabetic rats. Naringin and glibenclamide treated diabetic rats showed a significant low levels of AChE activity and TNF-&#945;. Conclusion: Naringin ameliorates diabetes induced cognitive deficit via reduction of inflammation, hyperglycemia, hyperlipidaemia and AChE activity</abstract>
	<keyword_fa>Naringin, Diabetes, Cognitive decline, Inflammation, Acetylcholinesterase.</keyword_fa>
	<keyword></keyword>
	<start_page>20</start_page>
	<end_page>29</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1374-2&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/12
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/2/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Abiodun</first_name>
	<middle_name></middle_name>
	<last_name>Oyindamola O</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>oo.abiodun@mail.ui.edu.ng</email>
	<code>00319475328460030718</code>
	<orcid>00319475328460030718</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Bakre</first_name>
	<middle_name></middle_name>
	<last_name>Adewale G</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030719</code>
	<orcid>00319475328460030719</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Adekoya</first_name>
	<middle_name></middle_name>
	<last_name>Christiana T</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030720</code>
	<orcid>00319475328460030720</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Kazeem</first_name>
	<middle_name></middle_name>
	<last_name>Adebola I</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030721</code>
	<orcid>00319475328460030721</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Oke </first_name>
	<middle_name></middle_name>
	<last_name>Tolulope A</last_name>
	<suffix></suffix>
	<affiliation>Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Ibadan, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030722</code>
	<orcid>00319475328460030722</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ujomu </first_name>
	<middle_name></middle_name>
	<last_name>Tejumade S</last_name>
	<suffix></suffix>
	<affiliation>Department of Anatomy, Physiology and Pharmacology, Lead City University, Ibadan, Nigeria</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030723</code>
	<orcid>00319475328460030723</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>The impact of sesamol and exercise on striatal TNF-α level, motor behavior, aversive memory and oxidative stress status in 6-hydroxydopamine-lesioned rats</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Neuroinflammation and oxidative stress play critical roles in the pathophysiology of Parkinson&#8217;s disease (PD), and neuroprotective agents could be helpful to slow down the dopaminergic neurodegeneration. Neuroprotective and antioxidant properties of exercise and sesamol have been previously reported. The current research evaluated the influences of sesamol and exercise on memory and motor impairments, oxidative stress and inflammatory markers in an experimental model of PD. Methods: 6-hydroxydopamine (6-OHDA) was microinjected into the medial forebrain bundle of male rats. Treatment with sesamol (50mg/kg) or treadmill exercise was performed for 7 weeks. Behavioral and biochemical assessments were performed at the end of 6th week after 6-OHDA injection. Results: Net number of rotations and tumor necrosis factor (TNF)-&#945; level was significantly enhanced in 6-OHDA group in comparison with sham group. Also, step-through latency was decreased in this group along with increased lipid peroxidation and decreased total thiol levels in the hippocampus. Moreover, sesamol and exercise, alone or in combination, improved rotational behavior, which was accompanied by decreased striatal TNF-&#945; level. However, sesamol and/or treadmill exercise had no effect on aversive memory, although exercise enhanced hippocampal total thiol level. Conclusion: Beneficial properties of sesamol and treadmill exercise for amelioration of motor impairments might be due to their anti-inflammatory activities.</abstract>
	<keyword_fa>Sesamol, 6-OHDA, Exercise, Motor activity, Memory, Oxidative stress.</keyword_fa>
	<keyword></keyword>
	<start_page>30</start_page>
	<end_page>38</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1220-3&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/19
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/29
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Somayeh</first_name>
	<middle_name></middle_name>
	<last_name>Shahidani</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030710</code>
	<orcid>00319475328460030710</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ziba</first_name>
	<middle_name></middle_name>
	<last_name>Rajaei</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>rajaeiz@med.mui.ac.ir</email>
	<code>00319475328460030711</code>
	<orcid>00319475328460030711</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hojjatallah</first_name>
	<middle_name></middle_name>
	<last_name>Alaei</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>alaei@med.mui.ac.ir</email>
	<code>00319475328460030712</code>
	<orcid>00319475328460030712</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Samaneh</first_name>
	<middle_name></middle_name>
	<last_name>Mohammadzadeh</last_name>
	<suffix></suffix>
	<affiliation>Poursina Hakim Digestive Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030713</code>
	<orcid>00319475328460030713</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>The protective effects of escitalopram on chronic restraint stress-induced memory deficits in adult rats</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Stress influences brain functions adversely but escitalopram exhibits positive effects on cognitive processes. Therefore, this study investigated the protective effects of different escitalopram doses on cognitive functions in rats under chronic stress and normal conditions. Methods: Forty-nine rats were randomly allocated into seven groups: control, sham, stress, escitalopram (10, 20 mg/kg/day) and stress-escitalopram (both doses). Initial latency, latency after 1-day, dark stay (DS) time and the number of entrances to the dark compartment were evaluated by passive avoidance test. Results: There were significant latency differences in stress and escitalopram10 groups compared to control group. Additionally, latencies showed significant enhancements in both 10 and 20 mg/kg/day stress-escitalopram groups compared to stress group and significant decrease in escitalopram20 group with respect to escitalopram10 group. DS time was significantly higher in stressed group and significantly lower in escitalopram10 groups, both compared to control group. Also, it was significantly lower in both stress-escitalopram groups in comparison with stress group. Furthermore, escitalopram20 group had a significantly higher DS time compared to escitalopram10 group. Finally, the number of entrances to the dark compartment was significantly lower in stress, escitalopram10 and stress-escitalopram10 groups compared to control group. Conclusion: Different doses of escitalopram affected brain functions under chronic stress and normal conditions. Escitalopram10 presented the most beneficial effects on improving brain functions under normal conditions. Whereas, both escitalopram doses showed similar protective effects on memory under stress. Overall, escitalopram at a dose of 10 mg/kg/day improved learning, memory consolidation and locomotor activity better than its maximum dose of 20 mg/kg/day.</abstract>
	<keyword_fa>Escitalopram, Stress, Learning, Memory, Passive avoidance.</keyword_fa>
	<keyword></keyword>
	<start_page>39</start_page>
	<end_page>48</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-895-7&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/8
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/18
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/12
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/23
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Zahra</first_name>
	<middle_name></middle_name>
	<last_name>Farahbakhsh</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030690</code>
	<orcid>00319475328460030690</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Maryam</first_name>
	<middle_name></middle_name>
	<last_name>Radahmadi</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>m_radahmadi@med.mui.ac.ir</email>
	<code>00319475328460030691</code>
	<orcid>00319475328460030691</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Evaluating the impact of Viola spathulata in a rat model of brain ischemia/reperfusion by influencing expression level of caspase-3 and cyclooxygenase-2</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Focal cerebral ischemia followed by reperfusion causes ischemia/reperfusion (I/R) brain injury. I/R injury is a complex pathophysiological process involving inflammation and apoptosis in neurons. Previous studies reported the anti-inflammatory traits of the family Violaceae. We aimed to evaluate the effects of Viola spathulata pre-treatment on infarct volume (IV), neurological deficit score (NDS) and alterations in mRNA level of cyclooxygenase 2 (COX2) and caspase 3 (CASP3) in a rat middle cerebral artery occlusion (MCAO) model. Methods: Thirty-three male Wistar rats were randomly distributed in 4 groups: normal control, MCAO control, MCAO + 5 mg/kg V. spathulata and MCAO + 10 mg/kg V. spathulata. Two doses of V. spathulata extracts were injected intraperitoneally for 7 days before the onset of ischemia. Finally, IV, NDS and mRNA expression of CASP3 and COX2 genes were assessed 24h after reperfusion. Results: IV and NDS in MCAO rats were remarkably higher compared with normal control rats and pre-treatment with V. spathulata extracts markedly reduced IV and NDS in the core, penumbra and subcortical regions of MCAO rats. Also, the level of COX2 and CASP3 mRNA was higher in the MCAO control group relative to normal control. Pre-treatment with V. spathulata extracts markedly reduced CASP3 mRNA relative to MCAO rats. Conclusion: It was found that V. spathulata might reduce ischemic damage in the brain of MCAO rats partly by decreasing apoptotic effects of CASP3. Further research is recommended to investigate signaling pathways involved in apoptosis.</abstract>
	<keyword_fa>Ischemia, Reperfusion, Viola spathulata, Caspase 3 (CASP3), Cyclooxygenase 2 (COX2)</keyword_fa>
	<keyword></keyword>
	<start_page>49</start_page>
	<end_page>59</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1466-1&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/7/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Mahsa</first_name>
	<middle_name></middle_name>
	<last_name>Ramezanpour</last_name>
	<suffix></suffix>
	<affiliation>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030692</code>
	<orcid>00319475328460030692</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Korosh</first_name>
	<middle_name></middle_name>
	<last_name>Khanaki</last_name>
	<suffix></suffix>
	<affiliation>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030693</code>
	<orcid>00319475328460030693</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Masomeh</first_name>
	<middle_name></middle_name>
	<last_name>Faezi</last_name>
	<suffix></suffix>
	<affiliation>Department of Medical Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030694</code>
	<orcid>00319475328460030694</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ekram</first_name>
	<middle_name></middle_name>
	<last_name>Mohammadi</last_name>
	<suffix></suffix>
	<affiliation>Department of Medical Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030695</code>
	<orcid>00319475328460030695</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Abbas</first_name>
	<middle_name></middle_name>
	<last_name>Gholipour</last_name>
	<suffix></suffix>
	<affiliation>Department of Biology, School of Sciences, Payame Noor University, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030696</code>
	<orcid>00319475328460030696</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mahmood</first_name>
	<middle_name></middle_name>
	<last_name>Abedinzade</last_name>
	<suffix></suffix>
	<affiliation>Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>mabedinzade@gums.ac.ir</email>
	<code>00319475328460030697</code>
	<orcid>00319475328460030697</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>The interactive effect of berberine chloride and exercise rehabilitation on the lung tissue apoptosis and oxidative stress biomarkers in rats exposed to diazinon</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: A serious complication of diazinon is the occurrence of oxidative stress in the respiratory system. The combination of medication and exercise rehabilitation has not been studied. The aim of this study was to assess the effects of berberine chloride alongside resistance training on apoptosis and oxidative stress markers of lung tissue in male rats exposed to diazinon. Methods: Forty-eight adult male Wistar rats were divided into 1: resistance exercise + berberine
chloride dose 2mg/kg + diazinon; 2: resistance exercise + berberine chloride dose 15mg/kg + diazinon; 3: toxic (diazinon 1.5 mg/kg); 4: resistance training + diazinon; 5: berberine chloride dose 2mg/kg + diazinon; 6: berberine chloride dose 15mg/kg + diazinon; 7: intact control and 8: normal saline. To induce oxidative stress, diazinon was injected intraperitoneally 1.5mg/kg. Berberine chloride was used as 2 and 15mg/kg through intraperitoneal injection for 4 weeks. Resistance training was conducted 3 sessions/week for 4 weeks including climbing a vertical ladder. Lung tissue was exposed to evaluate pathohistological test, apoptosis and oxidative stress markers. Results: Berberine chloride and exercise had a significant effect on decreasing ROS, MDA, caspase-3, and increasing GSH level, but no effect on the 8-OHDG. The exercise alone has no significant effect on ROS, MDA, 8-OHDG, caspase-3 and GSH. Conclusion: Berberine chloride alongside sport rehabilitation should be used as an effective treatment on lung apoptosis and oxidative stress with acute poisoning of diazinon. The most important mechanism is the effect of improving oxidative defense and anti-inflammatory effects.</abstract>
	<keyword_fa>Berberine chloride, Sport medicine, Apoptosis, Oxidative stress, Diazinon.</keyword_fa>
	<keyword></keyword>
	<start_page>60</start_page>
	<end_page>69</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1433-1&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/18
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/5/28
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Reza</first_name>
	<middle_name></middle_name>
	<last_name>Niazi</last_name>
	<suffix></suffix>
	<affiliation>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030698</code>
	<orcid>00319475328460030698</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Maghsoud</first_name>
	<middle_name></middle_name>
	<last_name>Peeri</last_name>
	<suffix></suffix>
	<affiliation>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>m.peeri@iauctb.ac.ir</email>
	<code>00319475328460030699</code>
	<orcid>00319475328460030699</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad Ali</first_name>
	<middle_name></middle_name>
	<last_name>Azarbayjani</last_name>
	<suffix></suffix>
	<affiliation>Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030700</code>
	<orcid>00319475328460030700</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Effect of nasal airflow on respiratory pattern variability in rats</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: The nasal airway a common route for normal breathing. Difficulty in nasal breathing due to nasal blockage is associated with abnormal respiratory pattern during sleep. The aim of this study was to investigate whether alteration in nasal airflow can change respiration pattern variability. Methods: Healthy male Wister rats were randomly divided into 4 groups including: control, saline, nasal obstruction and nasal cavity lidocaine anesthesia. The animals underwent bilateral nasal obstruction using cauterization and locally nasal cavity anesthesia using 10% lidocaine. Respiration of conscious animals recorded using whole-body plethysmography. Results: Respiratory signal analysis revealed a dramatic increase in variability of respiratory rhythm that quantified with increase in the standard deviation of inter-breath interval, inspiration time and mean of IBI, expiration and expiration to inspiration time ratio in both nasal obstruction and nasal anesthetized animals. Additionally, Power spectral density analysis showed higher variability in respiratory frequency, which characterized with broader dominant frequency and periodic respiratory pattern in nasal obstruction animals. Conclusion: These results proposed that, nasal airflow influences respiratory pattern variability. Nasal cavity flow receptors may contribute for these observations.</abstract>
	<keyword_fa>Nasal obstruction, Respiratory pattern, Nasal airflow, Apnea.</keyword_fa>
	<keyword></keyword>
	<start_page>70</start_page>
	<end_page>78</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1265-3&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/28
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/10/8
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/10
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/21
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Saeed</first_name>
	<middle_name></middle_name>
	<last_name>Pazhoohan</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>Saeedpazhoohan@yahoo.com</email>
	<code>00319475328460030701</code>
	<orcid>00319475328460030701</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Fatemeh</first_name>
	<middle_name></middle_name>
	<last_name>Abbasi Feijani</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030702</code>
	<orcid>00319475328460030702</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Farnaz</first_name>
	<middle_name></middle_name>
	<last_name>Mehrabbeigi</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030703</code>
	<orcid>00319475328460030703</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad Reza</first_name>
	<middle_name></middle_name>
	<last_name>Palizvan</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030704</code>
	<orcid>00319475328460030704</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Saeed</first_name>
	<middle_name></middle_name>
	<last_name>Hajihashemi</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030705</code>
	<orcid>00319475328460030705</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Selegiline induces adipose tissue-derived stem cells into neuron-like cells through MAPK signaling pathway</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Adipose-derived stem cells (ADSCs) are one of the most well-known and accessible sources of stem cells that can be used for the treatment of neurodegenerative diseases. On the other hand, previous studies have suggested that selegiline, as an irreversible inhibitor of monoamine oxidase, affects stem cells&#8217; differentiation into neurons. This study was conducted to investigate the involvement in phosphatidylinositol-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways in ADSCs differentiation to neuron-like cells using selegiline as inducer. Methods: ADSCs were isolated from male rats, cultured in DMEM and then treated with selegiline (10-7 M) for 24h. Real-time PCR for nestin and neurofilament-68 (NF-68) was performed from the negative control (ADSCs at the 3rd passage), positive control (ADSCs were treated with 10-7 M selegeline for 24h, PI3AKT inhibitor (ADSCs were pretreated with treated with 10&#181;M LY294002 for 3h, then10-7 M selegeline for the next 24h, and MAPK inhibitor (ADSCs were pretreated with treated with 10&#181;M PD98059 for 3h, then10-7 M selegeline for the next 24h). Results: Nestin and NF-68 genes have been over-expressed in the selegiline-treated ADSCs. The PD98059 and LY294002 significantly down-regulated the selegiline-induced over-expression of nestin and NF-68; however, PI3K inhibition did not return the genes expression to control level. ADSCs were immunoreactivefor nestin and NF-68 about 98% and 95% respectively. Conclusion: According to the results, selegilinecan induce the gene expression of neural stem cell biomarkers in ADSCs through MAPK pathway activating and so differentiating them into neuron-like cells.</abstract>
	<keyword_fa>Selegiline, Adipose-derived stem cells, Neuron-like cells, MAPK.</keyword_fa>
	<keyword></keyword>
	<start_page>79</start_page>
	<end_page>87</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-839-3&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/8/24
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Alireza</first_name>
	<middle_name></middle_name>
	<last_name>Abdanipour</last_name>
	<suffix></suffix>
	<affiliation>Department of Anatomical Sciences, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030706</code>
	<orcid>00319475328460030706</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Maedeh</first_name>
	<middle_name></middle_name>
	<last_name>Amalavar</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030707</code>
	<orcid>00319475328460030707</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohsen</first_name>
	<middle_name></middle_name>
	<last_name>Alipour</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030708</code>
	<orcid>00319475328460030708</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hadi</first_name>
	<middle_name></middle_name>
	<last_name>Feizi</last_name>
	<suffix></suffix>
	<affiliation>Department of Physiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>hfeizik@zums.ac.ir</email>
	<code>00319475328460030709</code>
	<orcid>00319475328460030709</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Diethylhexyl phthalate induced oxidative stress and caused metabolic imbalance in bone marrow mesenchymal stem cells</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Diethylhexyl phthalate (DEHP) is leaching form polyvinyl chloride to cause animal toxicity. In our previous study, DEHP caused osteoblasts mortality in vitro, since rat bone marrow mesenchymal stem cells (MSCs) is the cellular back up for osteoblasts; therefore its effect on MSCs was investigated. Methods: MSCs were extracted from Westar rats and treated with 0.5 to 2500&#956;M of DEHP for 12, 24 and 48h to study the viability. Then further investigations, including proliferation, cell morphology, sodium and potassium level, concentration of calcium, total protein, activity of metabolic enzymes (ALT, AST, ALP, LDH), malondialdehyde (MDA) level, total antioxidant capacity, activity of superoxide dismutase (SOD) and catalase (CAT) were measured using selected concentration (100, 500 and 1500&#956;M). Results: The 100&#956;M of DEHP did not change the viability and biochemical factor after 48h but colony forming assay and population doubling number was significantly affected. Th 500&#956;M only reduced the viability at 24 and 48h, while 1500&#956;M caused the significant reduction at all the periods. These two concentrations, caused significant proliferation reduction as well as significant increase in calcium and sodium level, LDH activity and MDA level. In addition, we observed decrease in potassium, total protein, activity of metabolic enzymes and activity of CAT and SOD significantly. Conclusion: DEHP has reduced viability and proliferation of MSCs through metabolic change, alteration in cellular ultrastructure, ionic imbalance and induction of oxidative stress.</abstract>
	<keyword_fa>Mesenchymal Stem Cell, Diethylhexyl phthalate, Oxidative stress, Cell survival, Enzymes assay.</keyword_fa>
	<keyword></keyword>
	<start_page>88</start_page>
	<end_page>100</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-432-2&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/142020/11/27
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1399/9/7
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/62021/04/6
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/1/17
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Mohammad Hussein</first_name>
	<middle_name></middle_name>
	<last_name>Abnosi</last_name>
	<suffix></suffix>
	<affiliation>Department of Biology, Faculty of Sciences, Arak University, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>m-abnosi@araku.ac.ir</email>
	<code>00319475328460030502</code>
	<orcid>00319475328460030502</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Zahra</first_name>
	<middle_name></middle_name>
	<last_name>Aliyari Babolghani</last_name>
	<suffix></suffix>
	<affiliation>Department of Biology, Faculty of Sciences, Arak University, Arak, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460030503</code>
	<orcid>00319475328460030503</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Corrigendum to “Antioxidant activity, phenolic and flavonoid content of Lawsonia inermis and Haplophyllum vermiculare” [Physiol Pharmacol 25 (2021) 261-269]</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Introduction: Continuous exposure of oxidants to the skin may disrupt the antioxidant balance and leads to inflammatory skin diseases (ISD). The aim of the present study was to compare the antioxidant activity, phenolic and flavonoid content of two traditionally used plants in ISD, Lawsonia inermis and Haplophyllum vermiculare.
Methods: The hydroethanolic extract of the plants was prepared by maceration. Phenolic and flavonoid content of the extracts was measured respectively with Folin-Ciocateu and aluminum chloride methods. The monovalent reducing power and radical scavenging activity were also evaluated respectively by ferric reducing antioxidant power and 2,2-diphenyl-1-picryl-hydrazyl methods.
Results: The reducing power of Lawsonia inermis (862.89&#177;32.23 &#956;molFe2+/g) was significantly higher than Haplophyllum vermiculare extract (765.52&#177;29.39 &#956;molFe2+/g). The radical scavenging activity of Lawsonia inermis extract at a concentration of 1000&#956;g/ml (%65.72&#177;0.77) was also significantly higher than Haplophyllum vermiculare (%36.34&#177;2.52). The higher antioxidant activity of Lawsonia inermis is probably due to its higher phenolic (96.76&#177;3.34&#956;g GAE/mg) and flavonoid content (197.69&#177;5.76&#956;g QE/mg).
Conclusion: Henna leaves had higher antioxidant activity, phenolic and flavonoid content compared to aerial parts of Haplophyllum vermiculare, and may be more effective in improving oxidative stress, prevention and treatment of ISD.</abstract>
	<keyword_fa>,Lawsonia inermis,Haplophyllum vermiculare,Antioxidative activity,Skin disease,Inflammation</keyword_fa>
	<keyword></keyword>
	<start_page>101</start_page>
	<end_page>101</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-1681-6&amp;slc_lang=en&amp;sid=1</web_url>
		<RECEIVE_DATE>
			2020/10/92021/01/232020/05/122020/12/192020/12/82020/10/142020/08/182020/12/282020/11/142020/11/272022/03/16
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1400/12/25
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2021/03/92021/04/102021/04/62021/04/102021/04/122021/04/62021/04/62021/04/102021/04/62021/04/62022/03/16
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1400/12/25
		</ACCEPT_DATE_FA>



		<author_list>
	<author>
	<first_name>Alireza</first_name>
	<middle_name></middle_name>
	<last_name>Moulazadeh</last_name>
	<suffix></suffix>
	<affiliation>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036642</code>
	<orcid>00319475328460036642</orcid>
	<coreauthor>
Yes
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Seyyed Amin</first_name>
	<middle_name></middle_name>
	<last_name>kouhpayeh</last_name>
	<suffix></suffix>
	<affiliation>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036643</code>
	<orcid>00319475328460036643</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Razieh</first_name>
	<middle_name></middle_name>
	<last_name>Ranjbar</last_name>
	<suffix></suffix>
	<affiliation>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036644</code>
	<orcid>00319475328460036644</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Amin</first_name>
	<middle_name></middle_name>
	<last_name>Dakhili Ardestani</last_name>
	<suffix></suffix>
	<affiliation>Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036645</code>
	<orcid>00319475328460036645</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Maryam</first_name>
	<middle_name></middle_name>
	<last_name>Hekmat</last_name>
	<suffix></suffix>
	<affiliation>Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036646</code>
	<orcid>00319475328460036646</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Sara</first_name>
	<middle_name></middle_name>
	<last_name>Azarnia</last_name>
	<suffix></suffix>
	<affiliation>Noncommunicable Disease Research Center, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>00319475328460036647</code>
	<orcid>00319475328460036647</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Sohrab</first_name>
	<middle_name></middle_name>
	<last_name>Najafipour</last_name>
	<suffix></suffix>
	<affiliation>Medicinal Plant Research Center, Fasa University of Medical Sciences, Fasa, Iran</affiliation>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>Najafipour.s@fums.ac.ir</email>
	<code>00319475328460036648</code>
	<orcid>00319475328460036648</orcid>
	<coreauthor>
No
	</coreauthor>
	<affiliation_fa></affiliation_fa>
	 </author>


		</author_list>


	</article>
</articleset>
</journal>
