动物造模 Z-bio 2023-02-08 635

　　Objective To investigate the myocardial protective effect of honokiol on acute myocardial infarction in mice and its possible regulatory mechanism.

　　Methods 80 male C57BL/6J mice were randomly divided into four groups, 20 in each group: sham operation (Sham) group, myocardial infarction model+vehicle (MI+V) group, myocardial infarction model+and magnolol treatment (MI+HKL) group, myocardial infarction model+and magnolol+sirtuin-1 (SIRT1) inhibitor (MI+HKL+EX) group. The death of mice within 28 days after modeling was recorded; On the 28th day after the operation, the mice were detected by echocardiography, and the animals were killed to take serum samples. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum inflammatory index. The cardiac tissue samples were taken, and the oxidative stress level of cardiac tissue was measured by dihydroethylidine (DHE) method, a reactive oxygen fluorescence probe; The apoptosis rate of myocardial cells was detected by terminal-deoxynucleotidyl transfer mediated nick end labeling (TUNEL) method, and the expression level of target protein was detected by Western blot.

　　Results Compared with the model group, HKL oral treatment after 4 weeks could significantly improve the cardiac function of myocardial infarction mice, reduce the level of serum inflammatory factors and the rate of myocardial apoptosis, reduce the level of myocardial oxidative stress, up-regulate the expression of SIRT1 and down-regulate the expression of Ac-Foxo1. However, after blocking SIRT1 signal with SIRT1 inhibitor EX527, the above protective effect of HKL was significantly reduced (P<0 05)。

　　Conclusion Oral administration of HKL can resist myocardial injury induced by myocardial infarction and significantly improve cardiac function in mice with myocardial infarction. The mechanism may be that SIRT1/Ac-Foxo1 signal is involved in regulation.