Faramarz Souri - Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad Badavi - Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Mahin Dianat - Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Seyyed Ali Mard - Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Alireza Sarkaki - Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Background: Serum and glucocorticoid-induced kinase ۱ (SGK۱) is an enzyme that may play an important role in ischemic-reperfusion (I/R) injury and myocardial dysfunction. Although many studies have been conducted on individual antioxidants, little attention has been paid to the effects of co-administration of an antioxidant with an SGK۱ inhibitor on cardiac function after I/R. Methods: This study aimed to determine the effects of gallic acid (as an antioxidant) combined with an SGK۱ inhibitor on I/R-induced cardiac dysfunction and inflammation. Sixty male Wistar rats were randomized into ۶ groups, pretreated with gallic acid or vehicle for ۱۰ days. Subsequently, the heart was isolated and exposed to I/R. In groups that received the SGK۱ inhibitor, the heart was perfused with the SGK۱ inhibitor GSK۶۵۰۳۹۴, ۵ min before induction of ischemia. After that, cardiac function, inflammatory factors, and myocardial damage were evaluated. Results: The combination of these two compounds improved cardiac contractility, heart rate, rate pressure product, left ventricular developed pressure, left ventricular systolic pressure, perfusion pressure, and QRS voltage significantly (P < ۰.۰۵). In addition, concomitant therapy of these two agents reduced tumor necrosis factor-alpha and interleukin-۶, and the activity of creatine kinase-MB, lactate dehydrogenase, and troponin-I (P < ۰.۰۵). Conclusions: The results indicated that administration of gallic acid with the SGK۱ inhibitor may have a potentiating effect on the improvement of cardiac dysfunction and I/R-induced inflammation.

Gallic Acid, Inflammation, Ischemic-Reperfusion Injury, Rat, Serum-glucocorticoid regulated kinase ۱ (SGK۱). ​​​​