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作 者:卫文博[1] 段大鹏[1] 孙正明[1] 徐洪海[1] 刘宗智[1] 弓立群[1] 常彦海[1] 李全义[1] 马战胜[1] 刘时璋[1] Wei Wenbo ,Duan Dapeng ,Sun Zhengming ,Xu Honghai ,Liu Zongzhi ,Gong Liqun ,Chang Yanhai ,Li Qua- nyi, Ma Zhansheng, Liu Shizhang.(Orthopedic Hospital of Shanxi People's Hospital, Xian 710068, Shaanxi, China)
机构地区:[1]陕西省人民医院骨科医院,陕西西安710068
出 处:《贵州医药》2018年第3期263-266,共4页Guizhou Medical Journal
基 金:陕西省科技统筹创新工程计划项目(编号2015KTCL03-02)
摘 要:目的探讨CCN2单克隆抗体对硬膜外瘢痕粘连的治疗作用及潜在机制。方法制备椎板切除模型大鼠,以CCN2单抗处理模型大鼠,观察其对大鼠硬膜外瘢痕粘连以及细胞外基质表达的影响。以TGF-β1处理原代成纤维细胞,观察CCN2单抗处理对模型细胞增殖活性、细胞外基质表达以及炎性因子分泌等的影响,检测CCN2单抗对模型细胞中TGF-β/Smads信号通路的影响。结果 CCN2单抗处理能明显改善模型大鼠硬膜外瘢痕粘连情况,降低瘢痕组织及模型细胞中Ⅰ型胶原、Ⅲ型胶原、α-SMA的表达水平(P<0.05)。同时,CCN2单抗还能抑制模型细胞的增殖活性,以及成纤维细胞生长因子FGF-2与IL-6的表达量,并能降低模型细胞中TGF-β2、TGF-β3的表达水平及p-Smad2的含量,差异有统计学意义(P<0.05)。结论 CCN2单抗处理可抑制成纤维细胞内TGF-β/Smads信号通路的活化,进而抑制成纤维细胞的过度增殖及炎性反应的发生,缓解硬膜外粘连症状。Objective To explore the therapeutic effect of anti-CCN2 monoclonal antibody to epidural adhesions and potential mechanism. Methods Rat lamina resection model were established and treated by anti-CCN2 monoclonal antibody to observe its effect on epidural scar adhesion and extracellular atrix expression. Primary fibroblasts were treated by TGF-131,and the effects of anti-CCN2 monoclonal antibody on cell proliferation activity,extracellular ma- trix expression and inflammatory cytokines secretion were detected. And the influence of anti-CCN2 monoclonal anti- body to the TGF-13/Smads signal pathway was also measured in fibroblasts. Results Anti-CCN2 monoclonal antibody can obviously improve the epidural cicatrix adhesion and reduce the expression of type I collagen, collagen type III and ^-SMA in the scar tissue and the model cells (P^0.05). Meanwhile, anti-CCN2 monoclonal antibody also inhibi- ted the proliferation activity of model cells, reduced the expression of fibroblast growth factor FGF-2 and IL-6, and decreased the levels of TGF-132,TGF-β3 and p-Smad2 in model cells (P〈0.05). Conclusion Anti-CCN2 monoclonal antibody can inhibit the activation of TGF-βSmads signal pathway in fibroblasts to reduce the excessive proliferation of fibroblasts and inflammatory reaction,contributing to the alleviation of epidural adhesions.
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