Tumstatin (69–88) alleviates heart failure via attenuating oxidative stress in rats with myocardial infarction

Abstract

BackgroundThis study aimed to elucidate the effects of tumstatin (69–88) on heart failure and the underlying mechanism. Materials and methodsMyocardial infarction (MI) was induced by ligating the left coronary artery in rats to trigger heart failure. ResultsTumstatin (69–88) can reduce cardiac insufficiency in rats with heart failure. The increased cardiac fibrosis in MI rat was attenuated by tumstatin (69–88). Increase of cardiac atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in rats with myocardial infarction, and Ang II-treated NRCMs or H9C2 cells was inhibited by tumstatin (69–88). In the heart of MI rats, and Ang II-treated NRCMs or H9C2 cells, the superoxide anions and NADPH oxidase (Nox) activity rose and the superoxide dismutase (SOD) activity was reduced, which was inhibited by tumstatin (69–88). Diethyldithiocarbamate, an SOD inhibitor, increased the ANP and BNP in NRCMs or H9C2 cells. Tumstatin (69–88) inhibited the Ang II-induced raises of ANP and BNP in NRCMs or H9C2 cells, which was reversed by DETC. ConclusionsThese results indicate that tumstatin (69–88) alleviates cardiac dysfunction of heart failure. Tumstatin (69–88) improves the hypertrophy of cardiomyocytes via attenuation of oxidative stress. Tumstatin (69–88) may be a potential drug for heart failure in the future.