[Animal Experiment]-Guanxinning Tablet inhibits cardiomyocyte apoptosis in mice with chronic heart failure through PI3K/AKT signaling pathway

  OBJECTIVE: To observe the therapeutic effects of Guanxinning tablets on chronic heart failure (CHF) mice, explore the pathways of cardiomyocyte apoptosis and related cell signaling pathways, and provide experimental evidence for the clinical application of Guanxinning tablets. is it?

  Method: Have you established a mouse CHF model through aortic arch stenosis, and successfully divided the model mice into a model control group? Guanxining tablets low-dose group (600mg/kg)? The high-dose group of Guanxining tablets (1200 mg/kg)) the captopril positive control group (12.5 mg/kg) and the sham operation group were the control groups. During the experiment, the survival rate of the animals will be observed, and ultrasound imaging will be performed 3 to 6 to 9 weeks after administration to detect the excretion rate of the mice. (EF) After the administration, the mice were slaughtered and the heart tissues were collected. The apoptosis of cardiomyocytes was observed by TUNEL method, and the mRNA expression of BAX and BCL2 genes was detected by RT-PCR method and automatic protein analyzer. Through PI3K? P-AKT is detected. And what about the protein expression level of BAX/BCL2?

  Result: The survival rate of mice in the model control group was 50%, that of the low-dose Guanxinning tablet group was 60%, and that of the high-dose Guanxinning tablet group was 70%. Compared with the sham operation group, the EF value of mice in the model control group was significantly reduced after 3-6-9 weeks of administration, while the degree of improvement after the administration of Guanxinning tablets was different. Pathological observation showed that the cardiomyocytes of the model control group were abnormal. With the increase in deaths, can Guanxinning Tablets effectively reduce the level of cardiomyocyte apoptosis? The relative expression of BAX gene mRNA in the myocardial tissue of the model control group mice was significantly increased, BCL2 decreased, and also significantly increased, which was consistent with protein expression, PI3K and p-AKT levels; compared with PI3K in the model control group? Is the expression of p-AKT protein and BAX mRNA in myocardial tissue of Guanxinning high-dose group decreased?

  Conclusion: Guanxinning tablets can improve the survival rate of CHF mice and improve the heart function of CHF mice. Does this mechanism of action reduce cardiomyocyte apoptosis and improve heart failure symptoms in CHF mice by inhibiting the activation of PI3K/AKT/BAX signaling pathway?