化瘀理肺方对肺纤维化大鼠肺组织miR-27a与α-SMA表达的影响  

The effect of Huayu Lifei formula on the expression of miR⁃27a andα⁃SMA in lung tissue of bleomycin⁃induced rat lung fibrosis model

作　　者：林凌桑 陈洁 李思广 张蕾 丁毅鹏[1,2,3] LIN Ling-sang;CHEN Jie;LI Si-guang;ZHANG Lei;DING Yi-peng(Hainan Hospital Affiliated to Hainan Medical University,Haikou 570311,China;Department of General Practice,Hainan General Hospital,Haikou 570311,China;Department of Respiratory and Critical Care Medicine,Hainan General Hospital,Haikou 570311,China)

机构地区：[1]海南医学院附属海南医院,海南海口570311 [2]海南省人民医院全科医学科,海南海口570311 [3]海南省人民医院呼吸与危重症医学科,海南海口570311

出　　处：《海南医学院学报》2023年第22期1689-1695,共7页Journal of Hainan Medical University

基　　金：海南省人民医院国家自然科学基金培育530工程青年项目(2021QNXM10);国家自然科学基金资助(82160011)。

摘　　要：目的:探究化瘀理肺方对博莱霉素诱导大鼠肺纤维的抑制作用与对miR-27a、α-SMA表达的影响。方法:将Wistar大鼠随机分成正常组、模型组和化瘀理肺方治疗组各10只。采用注射博莱霉素构建肺纤维化大鼠模型。化瘀理肺方治疗组在造模7 d后给与化瘀理肺方灌胃治疗7 d。于造模后第14天分组处死大鼠。取右肺进行HE染色,Masson染色和免疫组化观察α-SMA的表达。通过qRT-PCR检测miR-27a的表达,同时采用双荧光素酶报告基因技术检测miR-27a与ACTA2(α-SMA蛋白编码基因)的结合位点。结果:与模型组比较,化瘀理肺方治疗组大鼠肺组织的病理形态学变化明显减轻,肺泡炎及纤维化明显降低,肺组织中胶原沉积明显减少,α-SMA蛋白表达明显降低。同时,化瘀理肺方治疗组肺组织miR-27a表达显著上升,双荧光素酶报告基因证实miR-27a与ACTA2基因存在结合位点。结论:化瘀理肺方可以抑制博莱霉素诱导大鼠肺纤维化,其机制可能与促进miR-27a表达有关。Objective:To investigate the inhibitory effect of Huayu Lifyei Formula on bleomycin-induced rat pulmonary fi-brosis and its impact on the expression of miR-27a andα-SMA.Methods:Wistar rats were arbitrarily classified into the normal group,the model group,and the group treated with Huayu Lifyei Formula,each consisting of ten rats.Pulmonary fibrosis rat model was established by injecting bleomycin.Subsequent to the modeling,the Huayu Lifyei Formula treatment group was admin-istered Huayu Lifyei Formula via gavage for a period of 7 days.Rats were sacrificed on the 14th day after modeling.The right lung was taken for HE staining,Masson staining,and immunohistochemical observation of alpha-smooth muscle actin(α-SMA)ex-pression.The expression of miR-27a was measured by qRT-PCR,with the miR-27a binding site on ACTA2(the gene encodingα-SMA protein)confirmed using dual-luciferase reporter gene technology.Results:When compared to the model group,the Hua-yu Lifyei Formula treatment group showed considerable alleviation of pathological morphological changes in lung tissue,with sig-nificant reductions in alveolitis,fibrosis,collagen deposition in lung tissue,and the expression ofα-SMA protein.Meanwhile,the expression of miR-27a in the Huayu Lifyei Formula treatment group significantly increased,and the dual-luciferase reporter gene confirmed the binding site of miR-27a with the ACTA2 gene.Conclusion:Huayu Lifyei Formula can inhibit bleomycin-induced pulmonary fibrosis in rats,and its mechanism may be related to the promotion of miR-27a expression.

关 键 词：肺纤维化 化瘀理肺方 miR-27a Α-SMA 

分 类 号：R285.5[医药卫生—中药学]