Cardioprotective effects of co-administration of thymoquinone and ischemic postconditioning in diabetic rats
- سال انتشار: 1400
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 24، شماره: 7
- کد COI اختصاصی: JR_IJBMS-24-7_004
- زبان مقاله: انگلیسی
- تعداد مشاهده: 118
نویسندگان
Department of Cardiology, Gansu Gem Flower Hospital, Lanzhou, Gansu, ۷۳۰۰۶۰, China
Department of Cardiology, Xigu People’s Hospital,Lanzhou, Gansu, ۷۳۰۰۶۰, China
Department of Cardiology, Gansu Gem Flower Hospital, Lanzhou, Gansu, ۷۳۰۰۶۰, China
چکیده
Objective(s): Ischemia/reperfusion (I/R) is a leading cause of myocardial infarction (MI) injury, contributing to excess injury to cardiac tissues involved in inflammation, apoptosis, and oxidative stress. The present study was conducted to examine the effects of combined thymoquinone (TQ) with ischemic postconditioning (IPostC) therapy on apoptosis and inflammation due to I/R injury in diabetic rat hearts. Materials and Methods: A single dose injection of streptozotocin (STZ; ۶۰ mg/kg) was administered to thirty-two Wistar male rats to induce diabetes. Hearts were fixed on a Langendorff setting and exposed to a ۳۰ min regional ischemia subsequently to ۶۰ min reperfusion. IPostC was induced at the onset of reperfusion by ۳ cycles of ۳۰ sec R/I. ELISA, Western blotting assay, and TUNEL staining were applied to assess the cardioprotective effect of IPostC and TQ against I/R injury in diabetic and non-diabetic rats.Results: Administration of TQ alone in non-diabetic isolated hearts significantly diminished CK-MB, TNF-α, IL-۱β, and apoptosis and enhanced p-GSK-۳β and Bcl-۲ (p < ۰.۰۵). Following administration of TQ, the cardioprotective effects of IPostC by elevating p-GSK-۳β and Bcl-۲ and alleviating apoptosis and inflammation were reestablished compared with non-IPostC diabetic hearts. Conclusion: These results provide substantial evidence that co-administration of TQ plus IPostC can exert cardioprotective effects on diabetic myocardium during I/R damage by attenuating the inflammatory response and apoptosis.کلیدواژه ها
Apoptosis, Diabetes, Inflammation, Ischemic postconditioning, Polyphenolsاطلاعات بیشتر در مورد COI
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