摘要
目的研究双氢青蒿素干预肺纤维化的作用机制。方法构建博来霉素诱导的大鼠肺纤维化模型[1],造模后行灌胃治疗。用HE染色、Masson染色法观察大鼠肺组织病理变化,碱水解法检测羟脯氨酸含量,Ellisa法检测血清中TGFβ1(转化生长因子β1)含量,荧光定量PCR法检测TGFβ1、SMAD2、SMAD3基因表达,免疫组化法检测大鼠肺组织中TGFβ1、SMAD2/3、p SMAD2/3蛋白表达。结果双氢青蒿素可减轻肺纤维化模型大鼠肺组织炎症和纤维化程度,抑制TGFβ1、SMAD2、SMAD3基因表达和TGFβ1、SMAD2/3、p SMAD2/3蛋白表达。结论双氢青蒿素可能通过抑制TGFβ1-SMAD2/3通路干预肺纤维化。
Objective To study the mechanism of dihydroartemisinin on pulmonary fibrosis. Methods The model of pulmonary fibrosis was induced by bleomycin,and then given intragastric administration. The tissue changes were detected by HE staining and Masson staining,and hydroxyproline content was measured by alkali hydrolyzing process. Ellisa method was used to determine serum TGFβ1 content,and fluorescence quantitative PCR method and immunohistochemical method to detect lung tissue of rats TGFβ1- SMAD2 /3 signaling pathways in the protein and gene expression. Results From the pathological results,alveolar inflammation and fibrosis degree of the dihydroartemisinine group and the prednisone group was heavier than that of the control group( P〈0. 01),but significantly lighter than the model group and the solvent group( P〈0. 01). From Ellisa method results,TGFβ1 at each time point in the sham group were significantly lower than the other four groups( P〈0. 01). The immunohistochemical method results showed that the average optical density of TGFβ1,p SMAD2 /3 and SMAD2 /3 in the sham group at each time point were significantly lower than the rest groups( P〈0. 01). The three indicators of the dihydroartemisinin group and the prednisone group at each time point were lower than the model group and the solvent group( P〈0. 01). The results of fluorescence quantitative PCR method showed that the TGFβ1 gene expression quantity of the dihydroartemisinin group was lower than the model group at each time point( P〈0. 01). Conclusion Dihydroartemisinin could treat bleomycin-induced fibrosis in rats by inhibiting TGFβ1- SMAD2 /3 signaling pathways.
出处
《临床肺科杂志》
2016年第10期1828-1832,共5页
Journal of Clinical Pulmonary Medicine