动物造模,慢性心力衰竭 z-bio 2021-09-07 403

　　Objective: To observe the therapeutic effect of Guanxinning tablets on chronic heart failure (CHF) mice, and to explore the pathway of action from cardiomyocyte apoptosis and related cell signaling pathways, so as to provide experimental evidence for the clinical application of Guanxinning tablets.

　　Methods: Aortic arch constriction was used to establish a mouse CHF model. The successfully modeled mice were divided into model control group, Guanxinning tablet low-dose group (600mg/kg), and Guanxinning tablet high-dose group (1200mg/kg). ) And the captopril positive control group (12.5mg/kg), and set the sham operation group as the control. During the experiment, observe the animal survival rate, and perform ultrasound imaging at 3, 6 and 9 weeks after administration to detect the ejection fraction of mice (EF), after the end of the administration, the mice were sacrificed and the heart tissue was taken. The apoptosis of myocardial tissue was observed by the TUNEL method, the expression of BAX and BCL2 gene mRNA was detected by the RT-PCR method, and PI3K､p-AKT was detected by the automatic protein analyzer. And BAX/BCL2 protein expression level.

　　Results: The survival rate of mice in the model control group was 50%, the survival rate of the Guanxinning tablet low-dose group was 60%, and the survival rate of the high-dose Guanxinning tablet group was 70%. Compared with the sham operation group, the model control group mice were EF The value decreased significantly after 3, 6 and 9 weeks of administration. After the administration of Guanxinning tablets, there were different degrees of improvement; pathological observation showed that the model control group mice had more cardiomyocytes apoptosis, and Guanxinning tablets could effectively reduce Cardiomyocyte apoptosis level. The relative expression of BAX gene mRNA in the myocardial tissue of the model control group mice was significantly increased, BCL2 decreased, which was consistent with protein expression, and the levels of PI3K and p-AKT also increased significantly; compared with the model control group, The protein expression of PI3K､p-AKT and the mRNA expression of BAX in the myocardial tissue of Guanxinning high-dose group decreased.

　　Conclusion: Guanxinning tablets can increase the survival rate of CHF mice and enhance the cardiac function of CHF mice. Its mechanism of action may be to reduce the apoptosis of cardiomyocytes by inhibiting the activation of PI3K/AKT/BAX signaling pathways, thereby improving CHF Symptoms of heart failure in mice.