Abstract
In order to explore the possible mechanism of curcumin in the treatment of AF, we focused on the myocardial fibrosis in the pathogenesis of atrial fibrillation to explore whether curcumin could play a role in the treatment of AF by reducing myocardial fibrosis.Rats were given daily gavage of saline (control and AF groups) or curcumin (4 mL/kg, concentration: 50 mg/mL, curcumin groups) during days 4-28. The rat model of AF was induced by Ach - CaCl2, and evaluate the therapeutic effect of curcumin on the duration of AF rhythm, the degree of myocardial fibrosis and the secretion of inflammatory factors in serum. RNA-seq to explore the possible mechanism of curcumin alleviating myocardial fibrosis of AF. curcumin significantly inhibits the duration of AF and reduces the degree of left atrial fibrosis. ELISA results showed curcumin could significantly reduce the secretion of IL-17A, IL-1β, IL -6 and TGF-β1. Bioinformatics analyses revealed that the IL-17 signaling pathway are involved in the therapeutic mechanism of curcumin. Furthermore, The genes encoding Col1a1, Fasn, Pck1, Bmp10, IL33 and Figf were pivotal and possible key genes for the therapeutic mechanisms of curcumin.Curcumin can reduce the degree of left atrial fibrosis of AF and the secretion of inflammatory factors. The therapeutic effect of curcumin on AF was attributed to its effect on the IL-17 signaling pathway. Besides, COL1A1, FASN, PCK1, BMP10, IL33 and FIGF were the pivotal genes associated with mechanisms of action of curcumin on AF.
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