Cardioprotective effects of co-administration of thymoquinone and ischemic postconditioning in diabetic rats
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Updated: Oct 15, 2025
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Junchuan Ran1, Huanglin Xu2, Wenyuan Li1
1Department of Cardiology, Gansu Gem Flower Hospital, Lanzhou, Gansu, 730060, China.
Objectives:
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; 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.
Results:
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 (P<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.
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.
