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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 effect and mechanism of peroxisome proliferator-activated receptor (PPARγ) agonist on neurite outgrowth in vitro. Methods PPARγ agonist troglitazone (TGZ) and its inhibitor GW-9662 (GW) and JNK specific inhibitor SP 600125 (SP) were added to primary cultured fetal rat hippocampal neurons to study the effects of PPARγ agonist On axonal growth of hippocampal neurons, and the role of JNK pathway activation in this process. Results Activation of PPARγ by TGZ significantly prolonged the axon of hippocampal neurons (P <0.05). PPAR antagonist GW abolished TGZ promoting axonal growth. Activation of PPARγ activated JNK pathway, and JNK-specific inhibitor SP can significantly block TGZ-induced axonal growth (P <0.05), suggesting that TGZ-induced axonal growth dependent JNK pathway activation. Conclusion PPARr agonists can promote axonal growth in hippocampal neurons, and this effect depends on the activation of JNK pathway.