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目的探讨JNK磷酸化在As2O3诱导的弥漫大B细胞淋巴瘤细胞凋亡过程中的参与机制。方法人弥漫大B细胞淋巴瘤细胞株LY1随机分为5组:对照组、三氧化二砷低剂量、中剂量、高剂量组及JNK阻断剂SP600125组。对照组和三氧化二砷组细胞给予DMSO或三氧化二砷(1Μm,5μM和25μM)孵育20 h。SP600125组在三氧化二砷(25μM)孵育的同时加入SP600125(10μM)孵育。CCK-8测定各组LY1细胞活力情况,q PCR和Western Blot分析各组细胞中细胞凋亡蛋白Bax、Bcl2、Caspase9及JNK和p-JNK蛋白的表达变化情况。结果人弥漫大B细胞淋巴瘤细胞株LY1随着三氧化二砷作用浓度升高而活力逐渐降低,且各组之间具有显著的统计学差异性(P<0.01)。q PCR和Western Blot结果显示三氧化二砷各组细胞凋亡蛋白Bax和Caspase9表达升高,而Bcl2表达降低。同时,三氧化二砷组中p-JNK1/2表达明显增高。而SP600125组上述异常均得到部分恢复。结论 JNK磷酸化过程参与了三氧化二砷诱导的弥漫大B细胞淋巴瘤的细胞凋亡过程。
Objective To investigate the mechanism of JNK phosphorylation in As2O3-induced apoptosis in diffuse large B cell lymphoma. Methods Human diffuse large B cell lymphoma cell line LY1 was randomly divided into 5 groups: control group, low dose, medium dose and high dose of arsenic trioxide, and JNK inhibitor SP600125 group. The control group and arsenic trioxide group cells were incubated with DMSO or arsenic trioxide (1 μM, 5 μM and 25 μM) for 20 h. The SP600125 group was incubated with SP600125 (10 μM) while arsenic trioxide (25 μM) was incubated. The activity of LY1 cells in each group was determined by CCK-8. The expression of Bax, Bcl2, Caspase9, JNK and p-JNK proteins were analyzed by q PCR and Western Blot. Results The human large diffuse large B cell lymphoma cell line LY1 gradually decreased with the increase of the concentration of arsenic trioxide, and there was a significant statistical difference (P <0.01). q PCR and Western Blot results showed that the expression of Bax and Caspase9 in arsenic trioxide groups increased, while the expression of Bcl2 decreased. Meanwhile, the expression of p-JNK1 / 2 in arsenic trioxide group was significantly increased. The SP600125 group of these anomalies have been partially restored. Conclusion JNK phosphorylation is involved in the apoptosis of arsenic trioxide induced diffuse large B cell lymphoma.