论文部分内容阅读
目的：研究维药买朱尼对退变软骨细胞中 Wnt/β- catenin 通路的调控作用。方法从1周龄 SD 大鼠关节中分离培养原代软骨细胞，采用人白细胞介素1β诱导软骨细胞退变。取第2代退变软骨细胞，分为对照组、模型组和维药组，采用 CCK -8方法检测细胞增殖状况；采用实时荧光定量 PCR 和免疫印迹法检测 Wnt/β- catenin 通路中 Wnt-3a、β- catenin、GSK -3β的表达水平。结果与对照组相比，模型组中软骨细胞增值速率减慢（ P <0.05）。采用维药买朱尼刺激后，软骨细胞的增殖速度显著加快（ P <0.05）。Wnt -3a、β- catenin 和 GSK -3β在模型组中表达显著增强（ P <0.05），维药买朱尼能降低 Wnt -3a、β- catenin 和 GSK -3β的表达水平（ P <0.05）。结论维药买朱尼能通过调节 Wnt/β- catenin 通路来发挥其保护关节软骨细胞的作用。“,”Objective To study the regulatory function of Uygur medicine Maizhuni on Wnt/ β - catenin pathway in the degeneration process of rat chondrocytes. Methods Primary chondrocytes were isolated from one week old SD rats and treated with interleukin - 1β to induce chondrocyte degeneration. Chondrocytes of passage 2 were randomly divided into control group,model group and Maizhuni group. CCK - 8 assay was performed to detect cell proliferation;quantitative real - time PCR and Western blotting were used to determine the expression of Wnt - 3a,β- catenin and GSK - 3β in the Wnt/ β - catenin pathway. Results Compared to the control group,the proliferation of chondrocytes treated with IL - 1β was obviously decreased( P < 0. 05). Vut Maizhuni administration significantly promoted cell proliferation( P < 0. 05). The expression of Wnt - 3a,β - catenin and GSK - 3β was significantly enhanced in the model group( P < 0. 05). Vut Maizhuni treatment reduced the expres-sion levels of Wnt - 3a,β - catenin and GSK - 3β( P < 0. 05). Conclusion Uygur medicine Maizhuni can protect the chondrocytes against IL- 1β induced degradation by regulation of Wnt/ β - catenin pathway.