Effect of Gallic Acid Pretreatment and SGK۱ Enzyme Inhibition on Cardiac Function and Inflammation in a Rat Model of Ischemia-Reperfusion Injury

سال انتشار: 1402
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 73

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شناسه ملی سند علمی:

JR_RBMB-12-1_016

تاریخ نمایه سازی: 31 مرداد 1402

چکیده مقاله:

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.

کلیدواژه ها:

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

نویسندگان

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

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