中文摘要：

目的探讨细胞外信号调节激酶（ERK）信号通路在CXCL16诱导的CIA小鼠淋巴细胞增殖中的调控作用。方法CCK8法检测CXCL16对CIA小鼠淋巴细胞增殖的影响，ELISA法检测细胞上清中TNF-α及RANKL表达，WesternBlot检测p-Raf-1、p-ERK1/2蛋白的表达，同时观察MEK抑制剂对CXCLl6诱导的上述变化的影响。结果CXCL16对正常小鼠淋巴细胞增殖的刺激作用不明显，但CIA＋CXCLl6组淋巴细胞增殖能力明显高于CIA空白组及CIA＋CXCL16＋抑制剂组（P〈0．05）。CIA＋CXCL16组TNF—α水平明显高于其他各组（P〈0．01）。RANKL水平在CIA＋CXCL16组明显高于CIA空白组（P〈0．01），但与CIA＋CXCL16＋抑制剂组相比无明显差别。p-Raf-1／β—actin及p-ERK1/2／β—actin在CIA＋CXCL16组明显高于CIA空白组（P〈0．05）。结论CXCL16可能通过激活Raf／MEK／ERK信号通路，诱导CIA小鼠淋巴细胞增殖活化。

英文摘要：

Objective To study the effect of Raf/MEK/ERK signal pathway on CXCL16-induced proliferation of lymphocytes in CIA mice. Methods Effect of CXCL16 on proliferation of lymphocytes in CIA mice was detected by CCK8 assay. Expressions of TNF- ct and RANKL as well as p-Raf-1 and p-ERK1/2 protein in cell supernatant were detected by ELISA and Western blotting, respectively. Effect of MEK inhibitors on CXCL16-induced changes in expression of TNF- α and RANKL as well as p-Raf-1 and p-ERK1/2 protein in cell supernatant was observed. Results CXCL16 had no significant effect on proliferation of lymphocytes in normal mice. The proliferation level of lymphocytes was significantly higher in CIA＋CXCL16 group than in CIA blank and CIA＋CXCL16＋inhibitor groups （P〈0.05）. The TNF-α level was significantly higher in CIA＋CXCL16 group than in other groups （P〈0.01）. The RANKL level was significantly higher in CIA＋CXCL16 group than in CIA blank group（P〈0.01） with no significant difference between CIA＋CXCL16 and CIA＋CXCL16＋inhibitor groups. The expression level of p-Raf-1 and p-ERK1/2 was significantly higher in CIA＋CXCL16 group than in CIA blank group （P〈0.05）. Conclusion CXCL16 can induce proliferation of lymphocytes in CIA mice by activating the Raf/MEK/ERK signal pathway.