血管生成素样蛋白4(Angptl4)在肺纤维化过程中的作用  

Influence of angiogenin-like protein 4 on pulmonary fibrosis

作　　者：刘胜岗[1] 杨红忠[1] Liu Shenggang;Yang Hongzhong(The Diagnostic and Therapeutic Centre of Respiratory Diseases, Changsha Central Hospital, Changsha 410004, China)

机构地区：[1]长沙市中心医院呼吸病诊疗中心,410004

出　　处：《中国医师杂志》2018年第5期712-714,719,共4页Journal of Chinese Physician

摘　　要：目的探讨血管生成素样蛋白4(Angptl4)在肺纤维化过程中的作用,以期为肺纤维化提供新的治疗靶点。方法博莱霉素气管滴注诱导大鼠肺纤维化模型,通过Western blot和RT-PCR检测肺组织中Angptl4的表达。大鼠肺成纤维细胞(RLF)转染Angptl4-shRNA质粒,用Western blot和RT-PCR观察转染后RLF细胞胶原纤维表达量的变化。结果在博莱霉素诱导的大鼠肺纤维化模型中,Angptl4的表达上调。转染Angptl4-shRNA质粒的RLF细胞经TGF-β处理后,在不同的时间点,collagen-1和collagen-4的表达下降。结论抑制Angptl4的表达可以降低肺组织中胶原纤维的表达,从而延缓肺纤维化的进展。Objective To investigate the important role of angiogenin-like protein 4 （Angptl4） in pulmonary fibrosis and to provide a new therapeutic targets for pulmonary fibrosis. Methods We established the pulmonary fibrosis animal models in rat by tracheal instillation of bleomycin. Then, we detected the expression of Angptl4 through real-time polymerase chain reaction （ RT-PCR ） and Western Blot. Rat lung fibroblast （RLF） was transfeeted into Angptl4-shRNA plasmid. Then we detected the changed collagen expression in RLF cells after transfection through RT-PCR and Western blot. Results The expression of Angptl4 was up-regulated in the bleomyein-indueed rat pulmonary fibrosis model. The expression of both collagen I and collagen IV in RLF cells transfeeted with Angptl4-shRNA plasmids were down-regulated compared with control after TGF-β treatment. Conclusions Inhibiting the expression of Angptl4 can reduce the expression of collagen fibers in lung tissue, then delaying the progression of pulmonary fibrosis.

关 键 词：肺纤维化/病理学 血管生成素样蛋白4/代谢 胶原I型/代谢 胶原Ⅳ型/代谢 大鼠 

分 类 号：R563[医药卫生—呼吸系统]