PPARγ激动剂通过激活JNK通路促进海马神经元轴突的生长  

PPARγ Activation Promotes Axon Elongation by a Mechanism that Involved JNK Activation

作　　者：田中秋[1] 冯斌[2] 韩树生[2] 孙印臣[2] 刘少朋[2] 张晓娟[2] 袁进国[2] 王丽丽[2] 王鹏[2] 

机构地区：[1]承德医学院,067000 [2]解放军第251医院神经外科,张家口075000

出　　处：《医学研究杂志》2014年第6期85-88,共4页Journal of Medical Research

摘　　要：目的初步探讨过氧化物酶体增殖物激活受体(PPARγ)激动剂对体外培养海马神经元轴突生长的作用及其机制。方法通过向原代培养的胎鼠海马神经元中加入PPARγ激动剂曲格列酮(TGZ)及其抑制剂GW-9662(GW)以及JNK特异性抑制剂SP 600125(SP),以研究PPARγ激动剂对海马神经元轴突生长的作用,以及JNK通路的活化在此过程中的作用。结果TGZ活化PPARγ后能明显促进海马神经元轴突的延长(P<0.05)。PPARr拮抗剂GW消除了TGZ的促轴突生长作用。PPARγ活化后激活了JNK通路,且JNK特异性抑制剂SP能明显阻断TGZ的促轴突生长作用(P<0.05),表明TGZ诱导的促轴突生长作用依赖JNK通路的激活。结论 PPARr激动剂能促进海马神经元轴突的生长,且此作用依赖JNK通路的激活。Objective To investigate the role of the activted PPARγ by TGZ in the axonal growth in hippocampal neurons. Methods Hippocampal neurons were treated with TGZ in the presence or absence of the specific PPARγ antagonist GW 4662 （GW） and the JNK inhibitor SP600125 （SP） to evaluate the possible role of JNK in TGZ - induced axonal elongation. Results PPAR-y stimulation by TGZ induces axonal growth in hippocampal neurons. The use of GW9662, a specific PPARγ antagonist, and SP 600125, an inhibitor of JNK, prevented these changes. Conclusion PPARγ activation promoted axonal growth in rat hippocampal neurons, and this effect was mediated by the activation of JNK signaling pathway.

关 键 词：过氧化物酶体增殖物激活受体Γ 曲格列酮 JNK通路 轴突生长 PPARΓ 

分 类 号：Q291[生物学—细胞生物学]