[Abstract] Objective To observe the therapeutic effect of Guanxinning Tablets on doxorubicin-induced heart failure (HF) in rats, and to explore its action pathway from the perspective of cell pyroptosis, so as to provide reference for the clinical application of Guanxinning Tablets. Methods The 30 rats were randomly divided into normal control group, model control group, Guanxinning tablet low-dose group (600 mg/kg), Guanxinning tablet high-dose group (600 mg/kg) and digoxin group (0.05 mg/kg). ), 6 pieces per group, the rat HF model was induced by multiple intraperitoneal injections of doxorubicin, and the drug was administered at the same time as the model was established, and it was continuously administered by gavage for 9 weeks. The survival of the rats was recorded in the experiment. After the last administration, echocardiography was used to detect cardiac function indexes. After the rats were sacrificed, serum was collected to detect NT-proBNP, IL-1β and IL-18, and HE staining was performed on cardiac tissue to observe cardiomyopathy. Physical morphological changes, Masson staining was used to observe myocardial fibrosis and myocardial collagen volume fraction (CVF) was determined, RT-PCR was used to detect the mRNA expression of NF-κB, TXNIP, NLRP3, ASC, Caspase-1, IL-1β and IL-18. Results Compared with the normal control group, the IVSd, IVSs, LVPWs, SV, FS, EFand heart rate of the model control group were significantly reduced, LVIDs and ESV were significantly increased, myocardium showed significant pathological changes, fibrosis increased, and the mRNA expression of NF-κB, TXNIP, NLRP3, ASC, Caspase-1, IL-1β and IL-18 was significantly increased. Compared with the model control group, Guanxinning tablet significantly increased IVSs, SV, FS, EF and heart rate, significantly reduced LVIDs and ESV, improved myocardial pathological damage, reduced fibrosis, and reduced mRNA expression of NF-κB, TXNIP, NLRP3, ASC, Caspase-1, IL-1β and IL-18. Conclusion Guanxinning tablet can reduce doxorubicin damage to myocardium and enhance cardiac function in rats, and its mechanism may be to improve myocardial pyroptosis in rats by inhibiting the NLRP3/ASC/Caspase-1 pathway. |