CTRP3通过TGF-β1/Smad信号通路减弱肝星状细胞活性机制研究  

Mechanism of CTRP3 attenuating hepatic stellate cell activation through TGF-β1/Smad signal pathway

作　　者：徐志刚 曹罡[2] 程传涛[2] 卢乐[2] 侯宏义 XU Zhigang;CAO Gang;CHENG Chuantao(Xijing Hospital of Air Force Military Medical University,Xi'an 710032)

机构地区：[1]空军军医大学西京医院,西安710032 [2]西安交通大学第二附属医院,西安710004

出　　处：《陕西医学杂志》2020年第5期523-526,530,共5页Shaanxi Medical Journal

基　　金：国家自然科学基金资助项目(81270562)。

摘　　要：目的:探讨C1q肿瘤坏死因子相关蛋白3(CTRP3)在肝纤维化中的作用及机制。方法:外科手术中提取11例正常肝组织及11例肝纤维化组织,检测CTRP3在正常肝组织、肝纤维化组织及活化的肝脏星状细胞(HSC)中表达差异。使用大鼠肝星形细胞系HSC-T6过表达CTRP3,检测HSC-T6细胞的增殖和迁移能力的变化以及TGF-β1/Smad通路的改变情况。结果:CTRP3在纤维化肝组织及活化的肝脏星状细胞中低表达。CTRP3的过表达抑制了HSC-T6细胞的增殖和迁移,同时抑制了HSC中TGF-β1/Smad通路的活化。结论:CTRP3在肝纤维化过程中发挥重要作用,能够调控细胞的增殖和迁移,同时能够调控TGF-β1/Smad通路,表明CTRP3可能是肝纤维化治疗的新靶点。Objective:To explore the role and mechanism of C1 q tumor necrosis factor related protein 3(CTRP3)in liver fibrosis.Methods:11 cases of normal liver tissue and 11 cases of liver fibrosis tissue were extracted in surgery.The difference of CTRP3 expression in liver fibrosis tissue and activated hepatic stellate cell(HSC)was detected by immunohistochemistry.The changes of proliferation and migration ability of HSC-T6 cells and TGF-β1/Smad pathway were detected after overexpression of CTRP3 in HSC-T6 cell line.Results:The expression of CTRP3 was low in hepatic fibrous tissue and activated HSC.The overexpression of CTRP3 inhibited the proliferation and migration of HSC-T6 and the activation of TGF-β1/Smad pathway in HSC.Conclusion:CTRP3 plays an important role in the process of liver fibrosis.It can regulate the proliferation and migration of cells and the TGF-β1/Smad signal pathway,indicating that CTRP3 may be a new target of liver fibrosis treatment.

关 键 词：肝纤维化 肝星状细胞 C1q肿瘤坏死因子相关蛋白3 细胞增殖 细胞迁移 TGF-Β1/SMAD信号通路 

分 类 号：R657.34[医药卫生—外科学]