OBJECTIVE: To observe the therapeutic effect of Guanxinning Tablets on chronic heart failure (CHF) mice, and to explore its action pathway from myocardial cell apoptosis and related cell signaling pathways, so as to provide experimental basis for the clinical application of Guanxinning Tablets.
Methods: The CHF model of mice was established by coarctation of the aortic arch, and the mice with successful modeling were divided into model control group, low-dose Guanxinning tablet group (600 mg/kg), and Guanxinning tablet high-dose group (1200 mg/kg). ) and captopril positive control group (12.5mg/kg), and the sham operation group was set as the control. During the experiment, the survival rate of animals was observed, and ultrasound imaging was performed at 3, 6, and 9 weeks after administration, and the ejection fraction of mice was detected. (EF), after the administration, the mice were sacrificed to obtain cardiac tissue, the apoptosis of myocardial tissue was observed by TUNEL method, the mRNA expressions of BAX and BCL2 genes were detected by RT-PCR, and PI3K and p-AKT were detected by automatic protein analyzer. and BAX/BCL2 protein expression levels.
Results: The survival rate of mice in the model control group was 50%, the survival rate of the low-dose Guanxinning tablet group was 60%, and the survival rate of the high-dose Guanxinning tablet group was 70%. Compared with the sham operation group, the EF of the mice in the model control group was At 3, 6, and 9 weeks of administration, the values of β-α and β decreased significantly, and after administration of Guanxinning Tablets, there were different degrees of improvement; pathological observation showed that the myocardial cell apoptosis of the mice in the model control group was more, and Guanxinning Tablets could effectively reduce the apoptosis. Apoptosis level of cardiomyocytes. The relative expression of BAX gene mRNA in the myocardial tissue of the mice in the model control group was significantly increased, and BCL2 was decreased, which was consistent with the protein expression, and the levels of PI3K and p-AKT were also significantly increased; compared with the model control group, the The protein expression of PI3K and p-AKT and the mRNA expression of BAX in the myocardial tissue of Guanxinning high-dose group decreased.
Conclusion: Guanxinning tablets can improve the survival rate of CHF mice and enhance the cardiac function of CHF mice. The mechanism may be to reduce the apoptosis of cardiomyocytes by inhibiting the activation of PI3K/AKT/BAX signaling pathway, thereby improving CHF. Heart failure symptoms in mice.