摘要
目的:探讨c-Jun氨基末端激酶(JNK)信号通路对胰岛βTc3细胞脂性凋亡的影响及吡格列酮(PGZ)的干预作用.方法:采用游离脂肪酸(FFA)诱导小鼠βTc3细胞凋亡;以MTT法观察FFA对细胞生长的抑制作用;流式细胞术检测细胞凋亡率;免疫细胞化学和Western Blot法检测在FFA、特异性JNK抑制剂SP600125及PGZ作用下磷酸化JNK(p-JNK)、磷酸化c-jun(p-c-jun)的表达.结果:FFA对体外生长的βTc3细胞具有明显抑制作用,并可诱导细胞凋亡,JNK阻断剂及PGZ可显著减少这一过程引起的凋亡;且FFA诱导βTc3细胞凋亡伴随着JNK信号通路中p-JNK和p-c-jun的升高;用SP600125预处理细胞后,可明显减少p-JNK和p-c-jun的活化;而PGZ未能抑制FFA引起的JNK活化.结论:JNK信号通路参与了FFA诱导的小鼠βTc3细胞凋亡;PGZ可明显抑制胰岛βTc3细胞凋亡,但这一过程可能没有通过JNK信号通路.
AIM：To investigate the effects of JNK signaling pathway on lipoapoptosis in mouse βTc3 cells and the intervention of pioglitazone（PGZ）. METHODS：Free fatty acid（FFA） was used to induce the apoptosis of βTc3 cells. MTT assay was used to observe the inhibitory actions of FFA on βTc3 cells.The JNK inhibitor SP600125 and PGZ were used to protect βTc3 cells. The apoptotic rate of the cells was detected by flow cytometry. The expression of p-JNK,p-c-jun were detected by immunocytochemistry and Western Blot. RESULT The growth of the βTc3 cells were remarkably inhibited by FFA in vitro, and significant apoptosis was induced by FFA with the activation of p-JNK, p-c-jun. SP600125 and PGZ could inhibit the apoptosis significantly. But FFA -induced activation of p-JNK and p-c-jun was suppressed by the JNK inhibitor SP600125 but not PGZ. CONCLUSION ：JNK signaling pathway was involved in lipoapoptosis of βTc3 cells. PGZ could inhibit the apoptosis of βTc3 cells stimulated by free fatty acids, but the JNK signaling pathway is not involved in the mechanism.
出处
《第四军医大学学报》
CAS
北大核心
2009年第21期2302-2305,共4页
Journal of the Fourth Military Medical University
基金
陕西省科技攻关项目(No2003K10-G114)
西安市科学技术局科技计划项目(SF08002)
