Effect of icariin on rats with pulmonary fibrosis and its mechanism

Acta Universitatis Medicinalis Anhui 2020 12 v.55 1840-1844     font:big middle small

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Authors:An Yunxia; Zhang Xiaoju; Wang Zheng

Keywords:bleomycin;α-smooth muscle actin;Bcl-2/Bax ratio;basic fibroblast growth factor

DOI:10.19405/j.cnki.issn1000-1492.2020.12.005

〔Abstract〕 Objective To investigate the effects and mechanism of Icariin on pathological damage and inflammatory response of lung tissue in rats with pulmonary fibrosis. Methods The pulmonary fibrosis model was established with bleomycin(BLM). Rats were randomly divided into healthy control(HC) group、BLM+Icariin(20 mg) group(BI20)、BLM+Icariin(40 mg) group(BI40) and BLM+Icariin(80 mg) group(BI80); HE, TUNEL and Masson staining were used to detect pulmonary pathological injury and fibrosis in rats. Protein expression of Bcl-2, Bax, Caspase-3, Caspase-9, transforming growth factor-β(TGF-β1), α-smooth muscle actin(α-SMA), basic fibroblast growth factor(bFGF), vascular endothelial growth factor(VEGF) and VEGFR was detected by Western blot. Elisa was used to detect the levels of inflammatory factors interleukin-6(IL-6), tumor necrosis factor-alpha(TNF-alpha) and IL-10. Results Icariin could improve the integrity of pulmonary tissue structure and reduce the apoptosis rate(P<0.01), up-regulate Bcl-2/Bax ratio(P<0.01), down-regulate Caspase-3 and Caspase-9 protein expression(P<0.01), up-regulate expression of IL-6 and TNF-α(P<0.01), down-regulate expression of IL-10, inhibit collagen deposition(P<0.01) and the overexpression of bFGF, VEGF and VEGFR. Conclusion Icariin can improve damage of lung tissue and alleviate inflammation in BLM-induced pulmonary fibrosis rats by activating bFGF/VEGF/VEGFR pathway.