Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study

Introduction: Overexposure to heat conditions can affect the functioning of the cardiovascular system and may promote cardiovascular disorders. Heat shock induced myocardial injury via increasing endoplasmic reticulum responsemediated apoptosis. This study investigated the impact of pretreatment with Rosa canina (RC), a natural antioxidant, on myocardial damage induced by heat stress exposure and underlying mechanisms in cardiomyocytes in rats. Methods: Sixty adult male Wistar rats were allocated into five groups, including Control: received normal saline (NS), Heat Stress (HS), and HS+RC groups. Animals in the HS groups were subjected to heat stress (43 ºC) for 15 minutes once a day for two weeks. Animals in the HS+RC groups received three doses of RC (250, 500, and 1000 mg/mL) one hour before being subjected to heat shock. The endoplasmic reticulum (ER) transmembrane kinases, including PKRlike endoplasmic reticulum kinase (PERK), immunoreactivity of CCAAT/enhancerbinding protein homologous protein (CHOP), and eukaryotic translation initiation factor 2alpha (eIF2α) as well as caspase 8 were detected by Western blot. The levels of reactive oxygen species (ROS) were assessed. Moreover, histopathological changes and apoptosis were also assayed in the heart tissue by using histopathological and TUNEL assays. Results: Heat exposure increased the level of ROS and induced oxidative damage in the heart tissue. The results demonstrated that RC administration decreased the overproduction of ROS induced by heat stress in cardiomyocytes. Moreover, heat stress up regulated the expression of pPERK, peIF2α,and CHOP protein while pretreatment with RC decreased expression of ER stressrelated markers in cardiomyocytes. Besides, RC diminished heat stressinduced cellular damage and apoptosis associated with inhibition of caspase 8 activation, a proapoptotic protein in cardiomyocytes. Conclusion: These findings indicate that RC exerts a protective effect on heart tissue, at least in part,through inactivation of PERK/eIF2α/CHOP pathway or inhibition of ER stress and oxidative stress triggeredapoptosis in cardiomyocytes induced by heat stress.