JNK抑制剂SP600125对游离脂肪酸诱导β细胞凋亡的影响

Effects of JNK inhibitor SP600125 on free fatty acids-induced apoptosis in mouse β Tc3 cells

目的探讨c-Jun氨基末端激酶(JNK)抑制剂SP600125在游离脂肪酸(FFA)诱导的胰岛β细胞凋亡中的作用。方法采用MTT法观察FFA对小鼠βTc3细胞生长的抑制作用,流式细胞术观察细胞凋亡率,免疫细胞化学和Western blot法检测p-JNK、p-c-Jun在FFA作用下及SP600125阻断JNK信号通路情况下的表达。结果 FFA可诱导体外生长的βTc3细胞凋亡,与对照组比较明显增加(P<0.05)。FFA诱导βTc3细胞凋亡过程中,p JNK和p c Jun蛋白显著增加(P<0.05);用SP600125预处理βTc3细胞后,p JNK和p-c-Jun蛋白含量较未处理组明显减少(P<0.05)。结论 FFA可诱导小鼠βTc3细胞凋亡,凋亡过程通过JNK途径实现。

Objective To investigate the anti-apoptotic effects of JNK inhibitor SP600125 on apoptosls in mouse βTc3 cells. Methods MTT assay was used to observe the inhibitory effects of FFA on generation of βTc3 cells . The apoptotic rate of the cells was detected by flow cytometry. The protein expressions of p-JNK, p c Jun were detected by immunocytochemistry and Western blot. Results The growth of the βTc3 cells were obviously inhibited by FFA in vitro, and significant apoptosis was present. FFA induced activation of p JNK, p-c-Jun. As a JNK inhibitor, SP600125 suppressed FFA -induced activation of p-JNK and p c Jun. Conclusion FFA can inhibit the proliferation of mouse βTc3 cells and induce βTC3 cells apoptosis. The JNK signaling pathway is involved in the mechanism of FFA-induced apoptosis.