Mechanism of pterostilbene in improving myocardial injury after percutaneous coronary intervention through being targeted on miR-26a-5p

Abstract

Our study aimed to discuss the mechanism of pterostilbene in improving myocardial injury after percutaneous coronary intervention (PCI) through targeting miR-26a-5p. The myocardial cells were isolated from C57BL/6 mice. They were frozen in liquid nitrogen for reservation after they were passaged. The cell transfection was performed with miR-26a-5p depressor or lipofectamine 3000. The Ischemia-Reperfusion (I/R) model was established. They were divided into several sets including control set, I/R set, miR-26a-5p imitative set, miR-26a-5p depressor set and pterostilbene set. The presentation of GAPDH and miR-26a-5p was monitored with Real-time PCR. The proliferation was tested with Flow Cytometry (FCM). Caspase-3 activity was tested with spectrophotometry. The protein expression was monitored with Western blot assay. The level of IL-6 and TNF-α was tested with ELISA method. There was abnormal miR-26a-5p expression in the I/R model. The survival rate of myocardial cells was improved by upregulating miR-26a-5p. And expression of apoptotic protein as p53 was reduced and SOD activity was increased. Reactive oxygen species (ROS) level was reduced. The level of IL-6 and TNF-α was restrained. miR-26a-5p in I/R model was increased with pterostilbene notably. The myocardial injury was improved by pterostilbene through regulating miR-26a-5p. It could provide a brand-new scheme for treating myocardial injury after PCI.