雷公藤甲素通过转化生长因子-β1通路抑制百草枯诱导的肺纤维化机制  

Mechanism of triptolide inhibiting pulmonary fibrosis induced by paraqua through the transforming growth factor β1 pathway

作　　者：李全[1] 陈群[2] 陈宏[1] LI Quan;CHEN Qun;CHEN Hong(First Affiliated Hospital,Heilongjiang University of Chinese Medicine,Harbin 150040,China;Acheng People’s Hospital,Harbin 150300,China)

机构地区：[1]黑龙江中医药大学附属第一医院,哈尔滨150040 [2]哈尔滨市阿城区人民医院,哈尔滨150300

出　　处：《中华中医药杂志》2023年第2期815-818,共4页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家自然科学基金面上项目(No.81573863,No.81774197);黑龙江省博士后资助项目(No.LBH-Z15213);中国博士后科学基金地13批特别资助(No.2020T130178);黑龙江省中医药科研项目(No.ZHY19-004)。

摘　　要：目的:探讨雷公藤甲素(TPL)通过转化生长因子-β1(TGF-β1)通路抑制抑制百草枯(PQ)诱导的肺纤维化的可能机制。方法:选用SPF级昆明小鼠40只,雌雄各半。分为对照组、模型组、雷公藤甲素组、TGF-β1组,每组10只。通过细胞在显微镜下计数,用ELISA方法对TGF-β1含量进行检测。免疫组织化学检测E-cadherin和Vimentin。结果:对照组大鼠呼吸平稳,毛色光滑,皮肤光亮,活力强,精力充沛。与对照组比较,模型组表现为麻木、气短并伴有隆隆声、发色不规则、皮肤暗沉、活力明显下降、消瘦加重。与模型组比较,雷公藤甲素组的精神状态、食欲、毛色、体质量和活跃性均有改善。TGF-β1可以恢复受雷公藤甲素抑制的细胞迁移和侵袭。与对照组比较,模型组小鼠肺组织HYP含量、血清TGF-β1显著升高(P<0.05);与模型组比较,雷公藤甲素组及TGF-β1组HYP含量、血清TGF-β1均显著降低(P<0.05),TGF-β1逆转了雷公藤甲素的抑制作用。与对照组比较,模型组E-cadherin蛋白水平表达下调(P<0.05),Vimentin蛋白表达上调(P<0.05)。与模型组比较,雷公藤甲素组及TGF-β1组E-cadherin蛋白表达水平显著升高(P<0.05),Vimentin蛋白表达水平显著降低(P<0.05),且雷公藤甲素组优于TGF-β1组(P<0.05)。结论:雷公藤甲素可能通过抑制TGF-β1的表达来抑制百草枯诱导的肺纤维化。Objective: To explore the possible mechanism of triptolide(TPL) inhibiting pulmonary fibrosis induced by paraquat through transforming growth factor β1(TGF-β1) pathway. Methods: Forty SPF Kunming mice were selected,and male and female were equally divided. Four groups were divided: control group,model group,triptolide group and TGF-β1group,10 rats in each group. The cells were counted under a microscope and TGF-β1 content was detected by ELISA.Immunohistochemical detection of E-cadherin and Vimentin. Results: Rats in control group had smooth breathing,shiny skin,vigorous and energetic. Compared with the control group,the symptoms of the model group were numbness,shortness of breath with rumbling,irregular hair color,dark skin,decreased vitality,and emaciation. Compared with model group,mental state,appetite,hair color,body weight and activity were improved in triptolide group. TGF-β1 can restore cell migration and invasion inhibited by triptolide. Compared with the control group,HYP content in the lung tissue and serum TGF-β1 in the model group were significantly increased(P<0.05);Compared with model group,HYP content in the lung tissue and serum TGF-β1 in triptolide group and TGF-β1 group were significantly decreased(P<0.05),and TGF-β1 reversed the inhibition of triptolide.Compared with the control group,the expression of E-cadherin protein was down-regulated and the expression of Vimentin protein was up-regulated in the model group,with statistical significance(P<0.05). Compared with model group,E-cadherin protein expression in triptolide group and TGF-β1 group was significantly decreased(P<0.05),and Vimentin protein expression in TGF-β1 group was significantly increased(P<0.05),and triptolide group was superior to TGF-β1 group(P<0.05). Conclusion:Triptolide may inhibit paraquat-induced pulmonary fibrosis by inhibiting TGF-β1 expression.

关 键 词：雷公藤甲素 转化生长因子-Β1 百草枯 肺纤维化 

分 类 号：R285.5[医药卫生—中药学]