Title of article :
Antioxidant effects of amygdalin on tunicamycin-induced endoplasmic reticulum stress in the mice liver: Cross talk between endoplasmic reticulum stress and oxidative stress
Author/Authors :
Moslehi, Azam Cellular and Molecular Research Center - Qom University of Medical Sciences and Health Services , Komeili-movahed, Tahereh Cellular and Molecular Research Center - Qom University of Medical Sciences and Health Services , Moslehi, Mohammad Department of Pharmaceutics - School of Pharmacy - Shahid Beheshti University of Medical Sciences and Health Services
Pages :
5
From page :
298
To page :
302
Abstract :
Context: Both endoplasmic reticulum (ER) stress and oxidative stress are involved in pathophysiology of many diseases. Recently, a cross talk between ER stress and oxidative stress has been identified. Amygdalin is an active ingredient in the seeds of apricots, bitter almonds, peaches, and other rosaceous plants. Aim: This study was designed to evaluate the antioxidant effects of amygdalin on the liver-induced ER stress. Materials and Methods: C57/BL6 inbred male mice were placed in five groups comprising saline, vehicle, and amygdalin as control groups. ER stress was induced by tunicamycin (TM) injection (ER stress group). Amygdalin was administered 1h before TM challenge (ER stress + amygdalin group). Liver tissue supernatants were prepared and malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) were measured. Results: The findings showed that ER stress increased MDA level and decreased SOD and CAT activity and GSH level (P < 0.05). Pretreatment with amygdalin decreased MDA concentration, whereas it increased SOD and CAT levels (P < 0.05). Conclusion: This study showed that amygdalin attenuated TM-induced ER stress and has a considerable antioxidant activity in the liver tissue.
Keywords :
Amygdalin , endoplasmic reticulum , liver , oxidative stress , tunicamycin
Journal title :
Journal of Reports in Pharmaceutical Sciences
Serial Year :
2019
Record number :
2507099
Link To Document :
بازگشت