摘要
目的:观察扶正化纤方对博来霉素致小鼠肺纤维化的干预作用及可能机制。方法将96只 C57BL/6小鼠随机分为空白组、模型组、中药组和西药组4组。建立小鼠肺纤维化模型,除空白组外,其余各组分别应用扶正化纤方、N -乙酰半胱氨酸、生理盐水干预小鼠肺纤维化模型。采用免疫组化检测小鼠肺组织 IL -17A、TGF -β1的表达,QpCR 技术检测小鼠肺组织 IL -17A、TGF -β1 mRNA 的表达。结果免疫组化示:小鼠肺组织均可观察到 IL -17A、TGF -β1表达,定位在终末支气管和呼吸性细支气管、肺泡上皮,呈棕黄色阳性染色。阳性细胞 MOD 值分析显示:中药组14 d 和28 d 的 IL -17A、TGF -β1的表达均低于模型组、西药组(p <0.05)。QpCR 示:中药组 IL -17A mR-NA、TGF -β1 mRNA 的表达水平低于西药组、模型组(p <0.05)。结论“扶正化纤方”可能部分与下调 TGF -β1、IL -17A 的表达发挥抗纤维化作用。
Abstract
Objective To observe the intervention effect and mechanism of Fuzhenghuaxian decoc-tion with bleomycin - induced Pulmonary fibrosis in Mice. Methods 96 C57BL/ 6 mice were divided into blank grouP,model grouP,herb grouP and western medicine grouP. Pulmonary fibrosis animal model was es-tablished. ExcePt blank grouP,the other grouPs were treated with saline,Fuzhenghuaxian decoction and N -acetylcysteine resPectively. The lung tissue IL - 17A and TGF - β1 were detected with immunohistochemical method,and the exPression of IL - 17A and TGF - β1 mRNA were detected with QPCR method. Results Immunohistochemical results showed that IL - 17A,TGF - β1 exPression were observed in lung tissue of mice,Positioned at the terminal bronchioles,resPiratory bronchioles,and alveolar ePithelium. In Positive cells MOD value,the exPression of TGF - β1 and IL - 17A of herb grouP were lower than the model grouP,western medicine grouP(P < 0. 05). QPCR result showed that the exPression of TGF - β1 mRNA and IL - 17A mR-NA of herb grouP were lower than the model grouP,western medicine grouP(P < 0. 05). Conclusion Anti -fibrosis role of Fuzhenghuaxian decoction may be Partly related to reducing TGF - beta 1 and 17A - IL.