Rosmanol Alleviates Myocardial Ischemia-Reperfusion Injury by Enhancing the Myocardial miR-126/VEGF/PI3K/AKT Signaling in STZ-Induced Diabetic Rats.

Abstract

A major factor in type 1 diabetes mortality is Ischemic Heart Disease (IHD). In order to treat IHD, blood flow must be restored to the heart, which results in myocardial ischemia-reperfusion (MI/R) damage. While rosmanol inhibits MI/R damage, its role in diabetic- MI/R (D-MI/R) injury remains unclear. Both microRNA (miR) 126 and the PI3K/AKT signaling pathway have been linked to preventing MI/R damage. The objective of the present study was to investigate whether rosmanol inhibits DMI/ R-injury in diabetic rats and whether miR-126-phosphatidylinositol 3-kinase (PI3K)/ protein kinase B axis (miR-126-PI3K/AKT) is implicated in this protective effect. For 30 days, diabetic rats received either distilled water or the drug rosmanol (40 mg/kg, orally) before being subjected to MI/R. The findings from the current study demonstrated how rosmanol reduced MI/R damage in rats with diabetes caused by streptozotocin (STZ). Using spectrophotometry, it was possible to measure the decrease in myocardial enzyme levels, the rise in cardiac viability, the inhibition of myocardial oxidative stress, the increase in cardiac function, and the detection of these changes using a hemodynamic monitoring system. In addition, rosmanol augmented the miR- 126-PI3K/AKT in the hearts of ischemic rats. After stimulating the myocardial miR-126- PI3K/AKT axis, our results showed that rosmanol protected the heart against MI/R in STZinduced diabetic rats. According to the most recent research, rosmanol may be a useful tool in the therapy of diabetic IHD since it is an effective agent against D-MI/R damage.