Abstract
Background This study aimed to investigate the effect of miR-30c on myocardial ischemia reperfusion (IR) injury and its underlying molecular mechanisms.Methods In our study, rat myocardial IR injury model was established and hemodynamic examination was performed. Moreover, the myocardial infarct size was detected by TTC staining. The pathologic change of myocardial tissues was measured by HE staining. The myocardial cell apoptosis was measured by TUNEL staining and flow cytometry. The expression of miR-30c and Sirtuin 1 (SIRT1) was detected by qRT-PCR. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expressions of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 were detected by western blot. The luciferase activity was measured by dual luciferase reporter gene assay. Interaction between miR-30c and SIRT1 were analyzed by RNA immunoprecipitation assay.Results Our results showed that rat myocardial IR injury model was successfully established and IR injury induced myocardial injury in rats. miR-30c increased the levels of IL-1β, IL-6 and TNF-α and myocardial cell apoptosis by activating NF-κB pathway. In addition, we also confirmed that SIRT1 was the target gene of miR-30c. SIRT1 could reverse the effect of miR-30c on the process of inflammation and apoptosis, as well as the activation of NF-κB pathway in myocardial cells.Conclusions Our study demonstrated that miR-30c could promote myocardial ischemia reperfusion injury through activating SIRT1 mediating NF-κB pathway.
Sappanone A Prevents Left Ventricular Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model
