Found programs:
Authors:Sun Tao; Duan Jingsi; Gong Qian; Ge Shenglin; Chen Zhiwu
Keywords:ulinastatin;myocardial hypertrophy;autophagy;inflammation;isoproterenol
DOI:10.19405/j.cnki.issn1000-1492.2021.12.009
〔Abstract〕 Objective To investigate the protective effect of ulinastatin(UTI) on the myocardial hypertrophy induced by isoproterenol in rats and the possible mechanism. Methods Rat model of myocardial hypertrophy was established by subcutaneous injection of 5 mg/(kg·d) of isoproterenol for seven consecutive days. Ultrasound examination was used to detect cardiac function and myocardial hypertrophy; heart mass index(HMI) and left ventricular mass index(LVMI) were measured. Cardiac function and myocardial hypertrophy were measured by ultrasound. Myocardial tissue was examined by HE staining and Masson staining. Western blot was used to detect the expressions of autophagy protein Beclin-1, ATG-5, ATG-7, LC3-Ⅱ autophagy protein as well as inflammatory factor tumor necrosis factors(TNF)-α and interleukin(IL)-6. Results Compared with the ISO group, diastolic ventricular septal thickness, left ventricular posterior wall depth as well as HMI and LVMI in the UTI group significantly decreased, while left ventricular ejection fraction and left ventricular short axis shortening rate significantly increased; histopathological examination showed that UTI could significantly inhibit isoproterenol-induced myocardial injury and myocardial fibrosis; UTI could also significantly inhibit isoproterenol-increased protein expressions of TNF-α,IL-6 and autophagy-associated protein Beclin-1, ATG-5, ATG-7, LC3-Ⅱ in rat myocardium. Conclusion UTI significantly improves isoproterenol-induced cardiac dysfunction and myocardial hypertrophy in rats, which may be related to the inhibition of inflammation and autophagy.