en Toxicology Toxicology Experimental research article Experimental research article <div style="text-align: justify;"><span class="fontstyle0"><strong>Introduction:</strong> </span><span class="fontstyle2">Acrylamide (ACR) is a toxic substance that has renal toxicity. We aim to investigate the therapeutic activity of ellagic acid (EA) on renal injury induced by ACR in Wistar rats. </span><span class="fontstyle0"><strong>Methods:</strong> </span><span class="fontstyle2">Thirty-five male Wistar rats were assigned into 5 groups: the control group (5ml/kg normal saline), the ACR group (20mg/kg ACR), the ACR+EA10 group (ACR and 10mg/kg EA), the ACR+EA30 group (ACR and 30mg/kg EA) and the EA30 group (30mg/kg EA). ACR and EA were daily administered by gavage for 30 days. Renal function was assessed by measuring the sera levels of creatinine (Cr) and blood urea nitrogen (BUN). Renal oxidative and inflammatory markers including malondialdehyde (MDA), nitric oxide (NO), protein carbonyl (PC), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), tumor necrosis factor-&alpha; (TNF-&alpha;) and interleukin-1&beta; (IL-1&beta;). hematoxylin<br /> and eosin staining was employed to assess pathological alternations of the kidney. </span><span class="fontstyle0"><strong>Results:</strong> </span><span class="fontstyle2">EA (more potentially 30mg/kg) administration alleviated the ACR-induced alterations in Cr and BUN levels. Moreover, EA treatment reduced the elevated levels of MDA, NO and PC as well as TNF-&alpha; and IL-1&beta; content in renal tissue. Furthermore, reduced activity of SOD and CAT as well as GSH content in the kidney was increased by EA treatment. EA attenuated the ACR- induced pathological alterations in kidney. </span><span class="fontstyle0"><strong>Conclusion:</strong> </span><span class="fontstyle2">These findings suggested that EA could mitigate ACR-induced kidney injury due to its potent antioxidant and anti-inflammatory effects.</span></div> Acrylamide, Oxidative stress, Inflammation, Nephrotoxicity, Ellagic acid 313 321 http://ppj.phypha.ir/browse.php?a_code=A-10-873-3&slc_lang=en&sid=1 Saeed Mehrzadi 3200319475328460031314 3200319475328460031314 No Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran Mohammad Amin Mombeini 3200319475328460031315 3200319475328460031315 No Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Iman Fatemi 3200319475328460031316 3200319475328460031316 No Research Center of Tropical and Infectious Diseases, Kerman University of Medical Sciences, Kerman, Iran Heibatullah Kalantari 3200319475328460031317 3200319475328460031317 No Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Mojtaba Kalantar 3200319475328460031318 3200319475328460031318 No Shoushtar Faculty of Medical Sciences, Shoushtar, Iran Mehdi Goudarzi Goudarzi-M@ajums.ac.ir 3200319475328460031319 3200319475328460031319 Yes Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran