Abstract
OBJECTIVE: To explore the effect of microRNA-132 of heart failure and provide theoretical guidance for clinical treatment of heart failure (HF). METHODS: Peripheral blood was collected from HF patients. RT-qPCR was used to determine microRNA-132 expression. Mouse models of heart failure were established. Color Doppler ultrasound was utilized to measure the changes of cardiac function. HE and Masson staining were applied to observe pathological changes of the myocardium. After H(9)C(2) cells were transfected with microRNA-132, MTT assay was employed to detect the stability of H(9)C(2) cells. ELISA was used to measure the levels of oxidative stress factors. Western blot assay and RT-qPCR were utilized to determine the expression of Bax, Bcl-2, TGF-β1, and smad3. RESULTS: MicroRNA-132 expression was downregulated in HF patients' blood. After establishing mouse models of HF, cardiac function obviously decreased. HE staining revealed the obvious edema and hypertrophy of cardiomyocytes. Masson staining demonstrated that cardiomyocytes were markedly fibrotic. After microRNA-132 transfection and H(9)C(2) cell apoptosis induced by H(2)O(2), antioxidant stress and antiapoptotic ability of the H(9)C(2) cells obviously increased. TGF-β1 and smad3 expression remarkably diminished. CONCLUSION: Overexpression of microRNA-132 dramatically increased the antioxidant stress and antiapoptotic ability of H(9)C(2) cells and decreased the expression of TGF-β1 and smad3.