紫檀芪通过TLR4/NF-κB信号通路对肺纤维化大鼠的保护作用  

Protecive effect of pterostilbene on pulmonary fibrosis rats through TLR4/NF-kappaB signaling pathway

作　　者：彭艳芳[1] 张莹雯[1] 张亚兵[1] 柯浩亮[1] 王秀萍[1] PENG Yanfang;ZHANG Yingwen;ZHANG Yabing;KE Haoliang;WANG Xiuping(Dept.of Traditional Chinese Medicine,Zhongnan Hospital of Wuhan University,Wuhan 430071,Hubei,China)

机构地区：[1]武汉大学中南医院中医科,湖北武汉430071

出　　处：《武汉大学学报（医学版）》2022年第2期205-209,共5页Medical Journal of Wuhan University

基　　金：湖北省卫生计生委中医药科研基金面上项目(编号:ZY2019M080);第六批全国老中医药专家学术经验继承工作项目(国中医药人教发[2017]29号)。

摘　　要：目的:基于Toll样受体4(TLR4)/核转录因子-κB(NF-κB)信号通路观察紫檀芪(PTE)对博来霉素诱导的肺纤维化大鼠炎症反应和氧化应激的影响。方法:采用气管内注射博来霉素溶液制备大鼠肺纤维化模型。随机分为正常对照组、模型组、紫檀芪组(30 mg/kg)及强的松组(强的松3 mg/kg)。取肺组织进行Masson染色,试剂盒检测羟脯氨酸(HYP)含量、总抗氧化能力(T-AOC)及谷胱甘肽(GSH)表达水平,免疫组化法检测肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)、一氧化氮合酶(iNOS)的含量,Western Blot和PCR检测大鼠肺组织Toll样受体4(TLR4)、核转录因子-κB p65(NF-κB p65)的蛋白和mRNA的表达。结果:与模型组比较,紫檀芪组大鼠肺组织中HYP、TNF-α、IL-1β、iNOS蛋白表达量下降,T-AOC、GSH表达增强,TLR4和NF-κB p65的蛋白和mRNA表达水平明显下调。结论:紫檀芪能有效缓解肺纤维化,其机制可能与通过调控TLR4/NF-κB信号通路,抑制肺纤维化过程中的炎性因子、减弱氧化应激反应有关。Objective: To observe the effect of pterostilbene(PTE) on pulmonary fibrosis model rats.Methods: The rats were randomly divided into normal control group, model group, PTE group(PTE30 mg/kg), and prednisone group(prednisone 3 mg/kg). The rat pulmonary fibrosis model was prepared by intratracheal injection of bleomycin solution. Masson staining was performed on lung tissue.The total antioxidant capacity(T-AOC), hydroxyproline(HYP), and glutathione(GSH) expression levels in lung tissue were detected. TNF-α, IL-1β, and iNOS levels were detected by immunohistochemistry. Protein and mRNA levels of TLR4 and NF-κB p65 were detected by Western Blot and PCR respectively. Results: Compared with those in model group, the expression levels of HYP,TNF-α, IL-1β, and iNOS were decreased, T-AOC and GSH were increased, and the protein and mRNA levels of TLR4 and NF-κB p65 were significantly decreased. Conclusion: PTE can effectively alleviate pulmonary fibrosis, and its mechanism may be related to regulating TLR4/NF-κB pathway, inhibiting inflammatory factors in the process of pulmonary fibrosis, and weakening oxidative stress response.

关 键 词：紫檀芪 肺纤维化 TOLL样受体4 核转录因子-ΚB 

分 类 号：R563.9[医药卫生—呼吸系统]