Physiology and Pharmacology

en The effect of carvacrol on transcription levels of Bcl-2 family proteins in hypertrophied heart of rats Cardiovascular Physiology/Pharmacology Cardiovascular Physiology/Pharmacology Experimental research article Experimental research article Introduction: Cardiomyocytes apoptosis contributes to the development of left ventricular hypertrophy. The Bcl-2 family members are important regulators of mitochondrial pathway of apoptosis. Monoterpenoid phenol –carvacrol– possesses strong antioxidant properties. The present study aimed to evaluate the effect of carvacrol on transcription level of pro-apoptotic (Bad and Bax) and anti-apoptotic (Bcl-2 and BCL-xL) members of Bcl-2 family in hypertrophied hearts. Methods: Male Wistar rats (170-200 g) were divided into the following groups: (I) intact animals served as the control (Ctl), (II) un-treated rats subjected to aortic banding to induce left ventricular hypertrophy (H group), (III, IV, V and VI): carvacrol (C)-pretreated rats (5, 10, 25 and 50 mg/kg/day) subjected to aortic banding (H+C5, H+C10, H+C25 and H+C50 groups, respectively). Blood pressure was recorded through the carotid artery cannulation. Fibrosis was assessed by Masson’s trichrome staining. Gene expression was evaluated by real time-PCR technique. Results: In the H+C10, H+C25 and H+C50 groups mean arterial pressure (P<0.05, P<0.001 and P<0.001, respectively) and heart weight to body weight ratio (P<0.05, P<0.01 and P<0.001, respectively) were decreased significantly in comparison with H group. In the H group the Bad mRNA level was increased significantly compared to Ctl (P<0.001); while in the H+C10, H+C25 and H+C50 groups Bad mRNA level was decreased significantly (P<0.0 5, P<0.001 and P<0.001 vs. H). In H+C25 and H+C50 groups Bcl-2 and Bcl-xL mRNA were also up-regulated when compared with Ctl. Conclusion: Taken together, our results suggest that carvacrol may protect the hypertrophied heart against apoptosis by affecting transcription of Bcl-2 family members. Cardiac hypertrophy, Apoptosis, Carvacrol, Bcl-2, Bax, Bad, Bcl-xl 54 62 http://ppj.phypha.ir/browse.php?a_code=A-10-1023-1&slc_lang=en&sid=1 Sara Sadeghzadeh z.mohammadpour@stu.yazd.ac.ir 3200319475328460019152 3200319475328460019152 No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Seyed Hasan Hejazian s.hejazian@ssu.ac.ir 3200319475328460019153 3200319475328460019153 No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Mohabbat Jamhiri 3200319475328460019154 3200319475328460019154 No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Zeynab Hafizibarjin hafizi.219@ssu.ac.ir 3200319475328460019155 3200319475328460019155 No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Salman Sadeghzadeh salman.sdzd@iauashkezar.ac.ir 3200319475328460019156 3200319475328460019156 No Young Researchers and Elite Club, Yazd Branch, Islamic Azad University, Yazd, Iran Fatemeh Safari safarif@ssu.ac.ir 3200319475328460019157 3200319475328460019157 No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran