Ran Junchuan, Xu Huanglin, Li Wenyuan
Department of Cardiology, Gansu Gem Flower Hospital, Lanzhou, Gansu, 730060, China.
Department of Cardiology, Xigu People's Hospital,Lanzhou, Gansu, 730060, China.
Iran J Basic Med Sci. 2021 Jul;24(7):892-899. doi: 10.22038/ijbms.2021.47670.10981.
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.
A single dose injection of streptozotocin (STZ; 60 mg/kg) was administered to thirty-two Wistar male rats to induce diabetes. Hearts were fixed on a Langendorff setting and exposed to a 30 min regional ischemia subsequently to 60 min reperfusion. IPostC was induced at the onset of reperfusion by 3 cycles of 30 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.
Administration of TQ alone in non-diabetic isolated hearts significantly diminished CK-MB, TNF-α, IL-1β, and apoptosis and enhanced p-GSK-3β and Bcl-2 (<0.05). Following administration of TQ, the cardioprotective effects of IPostC by elevating p-GSK-3β and Bcl-2 and alleviating apoptosis and inflammation were reestablished compared with non-IPostC diabetic hearts.
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.
缺血/再灌注（I/R）是心肌梗死（MI）损伤的主要原因，会导致参与炎症、凋亡和氧化应激的心脏组织受到过度损伤。本研究旨在探讨胸腺醌（TQ）联合缺血后处理（IPostC）疗法对糖尿病大鼠心脏I/R损伤所致凋亡和炎症的影响。
对32只雄性Wistar大鼠单次注射链脲佐菌素（STZ；60mg/kg）以诱导糖尿病。将心脏固定在Langendorff装置上，先进行30分钟的局部缺血，随后再灌注60分钟。在再灌注开始时通过3个30秒的再灌注/缺血周期诱导IPostC。采用酶联免疫吸附测定（ELISA）、蛋白质免疫印迹分析和TUNEL染色来评估IPostC和TQ对糖尿病和非糖尿病大鼠I/R损伤的心脏保护作用。
在非糖尿病离体心脏中单独给予TQ可显著降低肌酸激酶同工酶（CK-MB）、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）水平并减少凋亡，同时增强磷酸化糖原合成酶激酶-3β（p-GSK-3β）和Bcl-2的表达（<0.05）。与未进行IPostC的糖尿病心脏相比，给予TQ后，IPostC通过升高p-GSK-3β和Bcl-2以及减轻凋亡和炎症所产生的心脏保护作用得以恢复。
这些结果提供了充分的证据，表明TQ与IPostC联合应用可通过减轻炎症反应和凋亡，对糖尿病心肌在I/R损伤期间发挥心脏保护作用。
