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目的探讨MAPK信号通路在交通相关PM2.5诱导CEM-6T细胞凋亡中的作用,为研究交通相关细颗粒物的免疫毒性机制提供实验依据。方法采用0、20、80、320mg/L PM2.5染毒CEM-6T细胞24、48h,用Western blot法检测交通相关PM2.5对CEM-6T细胞p-ERK、p-JNK和p38蛋白的作用;用p-JNK的拮抗剂SP600125和p38的拮抗剂SB203580进一步反面验证交通相关PM2.5是否影响CEM-6T细胞p-JNK和p38蛋白的表达。采用单因素方差分析进行数据分析。结果用不同剂量PM2.5(0、20、80、320mg/L)染毒CEM-6T细胞24、48h,随着染毒剂量增加,p-ERK蛋白表达量逐渐减少,320mg/L PM2.5组p-ERK蛋白表达量和生理盐水组比较明显降低,差异有统计学意义(P<0.05)。p-JNK1和p-JNK2蛋白表达量随染毒剂量增加而增加,320mg/L组与生理盐水组比较差异有统计学意义(P<0.05)。p38蛋白表达量随染毒剂量增加而增加,p38蛋白表达量在80和320mg/L PM2.5染毒组与生理盐水组比较差异有统计学意义(P<0.05);染毒前加入JNK拮抗剂(SP600125)和p38拮抗剂(SB203580)后,pJNK2和p38蛋白表达量均较正常染毒时降低,加与未加拮抗剂320mg/L PM2.5染毒组比较,差异有统计学意义。结论交通相关细颗粒物可能通过MAPK信号通路诱导CEM-6T细胞凋亡。
Objective To investigate the role of MAPK signaling pathway in the apoptosis of CEM-6T cells induced by traffic-related PM2.5, and to provide experimental evidence for studying the immunotoxicity mechanism of traffic-related fine particles. Methods CEM-6T cells were exposed to 0, 20, 80 and 320mg / L PM2.5 for 24 and 48 hours respectively. The expression of p-ERK, p-JNK and p38 proteins in CEM-6T cells The effects of p-JNK antagonist SP600125 and p38 antagonist SB203580 on the expression of p-JNK and p38 protein in CEM-6T cells were further verified by flow cytometry. One-way analysis of variance was used for data analysis. Results CEM-6T cells were exposed to different doses of PM2.5 (0, 20, 80, 320 mg / L) for 24 and 48 hours. The expression of p-ERK decreased with the dose of 320, Compared with the saline group, the expression of p-ERK protein was significantly decreased (P <0.05). The expression of p-JNK1 and p-JNK2 protein increased with the dose of 320 mg / L and the saline group had significant difference (P <0.05). The expression of p38 protein increased with the increase of dose. The expression of p38 protein was significantly different between PM2.5 group and normal saline group (P <0.05) at 80 and 320mg / L, and JNK antagonist (SP600125) and p38 antagonist (SB203580), the expression of pJNK2 and p38 protein were lower than those of the normal control group. The difference was statistically significant compared with the control group without the antagonist 320mg / L PM2.5. Conclusion Traffic-related fine particles may induce apoptosis of CEM-6T cells through MAPK signaling pathway.