外源性白介素24促进C6细胞凋亡的体外研究  

Exogenous interleukin 24 promotes apoptosis of rat glioma C6 cells

作　　者：李明辉[1] 赵静雅[2] 闫蕴力[3] 冯运章[1] 

机构地区：[1]邯郸市中心医院普外二科,河北邯郸056001 [2]邯郸市中心医院病理科,河北邯郸056001 [3]河北医科大学细胞生物学教研室,河北石家庄050017

出　　处：《实用肿瘤杂志》2016年第2期122-126,共5页Journal of Practical Oncology

摘　　要：目的探讨外源性白细胞介素24(interleukin 24,IL-24)体外抑制胶质瘤细胞增殖及促凋亡的相关机制。方法应用MTT体外观察转染IL-24对胶质瘤C6细胞增殖的抑制作用。应用Hoechst 33258荧光染色体外观察IL-24对C6细胞的促凋亡作用。Western blot法检测c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)和caspase-3蛋白的表达变化情况。结果 IL-24能使C6细胞的体外增殖能力降低,转入IL-24的C6细胞(C6/IL-24)增殖能力下降。经Hochest 33258染色,转入IL-24的C6细胞凋亡后出现核固缩、染色质凝集呈块或碎裂状改变。与转入空载体的C6细胞(C6/p LXSN)及C6细胞比较,C6/IL-24细胞的JNK和caspase-3蛋白表达均增高(均P<0.05)。C6/p LXSN与C6细胞比较差异无统计学意义(P>0.05)。结论外源性IL-24基因可抑制C6胶质瘤细胞的增殖并诱导其凋亡,该诱导凋亡的作用可能与其上调并激活JNK及caspase-3表达有关。Objective To investigate the mechanism of exogenous interleukin 24（ IL-24） inhibiting the proliferation and promoting the apoptosis of rat glioma C6 cells. Methods IL-24 gene was transfected to rat glioma cells. MTT was used to examine the proliferation of IL-24-transfected C6 cells（ C6/IL-24 cells）; Hoechst 33258 fluorochrome staining was adopted to analyze cell apoptosis; Western blot was used to detect the expression of c-Jun N-terminal kinase（ JNK） and caspase-3 proteins. Results MTT demonstrated that the proliferation rates of C6/IL-24 cells were significantly decreased（P〈0. 05）. Hoechst 33258 staining showed marked morphological changes in C6/IL-24 cells,as karyopyknosis,chromatin condensation and karyorrhexis. Compared with empty vector transfected cells（ C6/pLXSN cells） and un-transfected C6 cells,the levels of JNK and caspase-3 were both upregulated in C6/IL-24 cells（ P〈0. 05）; no significant difference was observed between C6/LXSN and C6 control cells（ P〉0. 05）. Conclusion Exogenous IL-24 expression inhibits the proliferation of C6 glioma cells and induces cell apoptosis,which is associated with the up-regulation of JNK and caspase-3 pathway.

关 键 词：神经胶质瘤/病理学 白细胞介素类/药理学 细胞系 肿瘤 半胱氨酸天冬氨酸蛋白酶3 JNK丝裂原活化蛋白激酶类 细胞凋亡/药物作用 细胞增殖/药物作用 

分 类 号：R739.41[医药卫生—肿瘤]