肺痹汤含药血清对IL-17诱导的MRC-5的影响及机制研究

Research on the influence and mechanism of pulmonary Feibi decoction contains serum for IL-17 induction of mrc-5

目的基于Smad通路研究肺痹汤含药血清对白细胞介素17(IL-17)诱导的人胚肺成纤维细胞二倍体(MRC-5)的影响,探讨肺痹汤防治肺间质纤维化的机制。方法建立IL-17诱导的MRC-5模型,通过CCK-8法检测细胞增殖水平,ELISA法检测TGF-β1、Smad 3、Smad 7表达水平,q PCR法检测Ⅰ型、Ⅲ型胶原蛋白RNA表达水平,研究肺痹汤含药血清对MRC-5模型是否具有干预效果。结果以IL-17诱导MRC-5细胞能够成功建立肺纤维化模型,肺痹汤含药血清对IL-17诱导的MRC-5细胞中Smad 3、Smad 7、TGF-β1、Ⅰ型胶原蛋白RNA、Ⅲ型胶原蛋RNA表达水平有明显下调作用。结论肺痹汤含药血清可抑制成纤维细胞的增殖,减少TGF-β1的分泌,阻断TGF-β1/Smad信号通路,从而减少胶原的合成与分泌,减轻纤维组织增生,从而改善肺间质纤维化。

Objective Based on Smad pathway to study the Feibi decoction drug-containing serum of interleukin 17 （IL-17） induction of crab,Tonic lung fibroblasts diploid （MRC - 5）, the influence of Feibi Decoction prevention mechanism of puhnonalT fibrosis. Methods MRC-5 induced by IL-17 model is set up, the level of cell proliteration by CCK 8 method and ELISA method to detect TGF - beta 1, Smad 3, Smad 7 expression level, I qPCR method, 11I RNA expression level of collagen, the Feibi decoction drug- containing sermn on whether MRC-5 models have intervention ettect. Results Induced by IL-17 MRC-5 cells can successthlly established puhnonalT fibrosis model, Feibi Decoction drug-containing sermn on the MRC-5 cells induced by IL-17 Smad 3, Smad 7, TGF - beta 1, I RNA collagen, collagen type 11I egg RNA expression level was obviously lowered. Conclusion Feibi decoction medicated sermn inhibits the proliteration of fibroblasts, reduce the secretion of TGF - beta 1, block TGF-beta l/Smad signaling path- ways, thereby reducing the synthesis and secretion of collagen, relieve hyperplasia of fibrous tissue, im- prove puhnonary interstitial fbrosis.