Chrysin restores the cardioprotective effect of ischemic preconditioning in diabetes-challenged rat heart

Background: Ischemic preconditioning (IPC) is the utmost capable design to achieve protection over ischemia-reperfusion injury (I/R), but this phenomenon gets attenuated during various pathological conditions like diabetes. Chrysin exhibits cardioprotection in various experiments however, its therapeutic potential on IPC-mediated cardioprotection via PI3K-Akt-eNOS pathway in streptozotocin (STZ) triggered diabetes-challenged rat heart is yet to be assessed. For that reason, the experiment has been planned to investigate chrysin's effect on the cardioprotective action of IPC involving the PI3K-Akt-eNOS cascade in rat hearts challenged to diabetes. Methods: The project was accomplished through means of absorbance studies for biochemical parameters, infarct size measurement (TTC stain) and coronary flow.Results: The findings of the present study revealed that STZ drastically augmented the serum glucose level and the chrysin significantly reversed the IPC-stimulated increased coronary flow, nitrite release, and reduced LDH (lactate dehydrogenase), CK-MB (creatine kinase) activities as well as infarct size in diabetes-induced rat heart. Furthermore, chrysin also reversed the IPCinduced reduction in oxidative stress in an isolated Langendorff's perfused diabetic rat heart. Moreover, four episodes of preconditioning by either PI3K or eNOS inhibitor in chrysin-pretreated diabetic rat hearts significantly abolished the protective effect of chrysin. Conclusion: Consequently, these observations suggested that chrysin increases the therapeutic efficiency of IPC in mitigating I/R injury via PI3K-Akt-eNOS signalling in diabetes-challenged rat hearts. Hence, chrysin could be a potential alternative option to IPC in diabetic rat hearts.

Automated summary

The study found that chrysin enhances the therapeutic effect of ischemic preconditioning (IPC) in diabetic rat hearts via the PI3K-Akt-eNOS signaling pathway, reducing ischemia-reperfusion injury.