The Shenlian Fumai Granule attenuates Ach-CaCl(2)-induced atrial fibrillation by regulating atrial electrical and structural remodeling.

BACKGROUND: Preliminary clinical studies indicate that Shenlian Fumai Granule (SLFM) reduces the incidence of arrhythmias following radiofrequency ablation in patients with atrial fibrillation (AF) and improves clinical symptoms. This study investigates the preventive effects and underlying mechanisms of SLFM on AF, providing robust evidence to support its clinical application. METHODS: The potential therapeutic effects of SLFM on AF were investigated using network pharmacology. Subsequently, High Performance Liquid Chromatography-Mass Spectrometry (HPLC-MS) was employed for further analysis of SLFM, while molecular docking was utilized to validate potential targets. The impact of SLFM on the electrophysiology of rat hearts was examined during Langendorff perfusion through electrical mapping. AF in rats was induced using Ach (66†μg/mL) and CaCl(2) (10†mg/kg), with a dose of 0.1†mL/100†g injected into the tail vein for a duration of 5 weeks. SLFM was administered daily at doses of 3.645 and 7.29†g/kg, with amiodarone (0.18†g/kg) serving as the positive control. The effects of SLFM on AF were assessed through electrocardiography, echocardiography, ELISA, and histopathological analysis. RESULTS: A total of 107 active compounds were extracted, and their relationships with Traditional Chinese Medicines (TCMs) and protein targets were analyzed. The intersection of potential TCM target genes and genes related to AF identified four significant genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these targets may be involved in various pathways associated with AF. Furthermore, SLFM was found to prolong the atrial effective refractory period in a concentration-dependent manner, suggesting a potential anti-atrial arrhythmia effect. In a rat model of AF induced by Ach-CaCl(2), SLFM treatment significantly reduced markers related to atrial electrical remodeling, including the induction rate and duration of AF, while also alleviating fibrosis and the upregulation of Connexin 43 (Cx43) expression. CONCLUSION: This study demonstrated that SLFM plays a critical role in suppressing atrial electrical and structural remodeling induced by Ach-CaCl(2), thereby further reducing susceptibility to AF. Consequently, SLFM may hold potential as a therapeutic agent for the treatment of AF.