Effect of apelin-13 on myocardial fibrosis in rats induced by pressure overload and TGF-β₁/ Smads pathway

Objective To study the effect of apelin-13 on myocardial fibrosis in rats induced by pressure overload and clarify its mechanism. Methods Forty SD rats were randomly divided into sham-operation group, model group, apelin-13 group and SB431542 group, 10 in each group. Rats in the sham-operation group were only separated their abdomens aorta. The other three groups were made into the model of myocardial fibrosis successfully. Three days after modeling, rats in different groups were given corresponding medication interventions. 4 weeks later, their cardiac index and left ventricular mass index (LVMI) were estimated. Morphology of collagen in myocardial tissue was observed with Masson staining, collagen volume fraction (CVF) in left ventricular interstitial tissue was measured by image analysis and the serum transforming growth factor β₁(TGF-β₁) expression was detected using ELISA and expressions of TGF-β₁protein, the collagen Ⅰ, Ⅲ were detected by Western-blotting. The Smad3 and Smad7 mRNA in myocardial tissue expressions were detected using real-time PCR. Results Compared with the Sham group, the cardiac index, LVMI, CVF in left ventricular interstitial tissue and the serum TGF-β₁level of the AOB group significantly increased (P＜ 0.05) and the TGF-β₁, the collagen Ⅰ, Ⅲ protein expression levels were significantly higher than that of the Sham group (P＜ 0.05). Compared with the AOB group, the cardiac index, LVMI, CVF, the serum TGF-β₁level obviously decreased (P＜ 0.05) and the TGF-β₁, the collagen fibers Ⅰ and Ⅲ expression levels significantly declined (P＜ 0.05) in the Apelin-13 group and the SB431542 group. The Smad7 mRNA expression in each group displayed contrary tendency. Conclusion Apelin-13 can alleviate myocardial fibrosis induced by pressure overload in rats through partially inhibiting TGF-β₁-Smads signal pathway.