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目的探讨交通相关PM2.5对大鼠脾脏细胞凋亡信号分子的影响,为研究交通相关PM2.5的免疫毒性机制提供实验依据。方法大鼠气管滴注不同剂量[1.5mg/(kg.d),6mg/(kg.d),24mg/(kg.d)]交通相关PM2.5和生理盐水对照,隔天染毒共6次,制备大鼠亚急性免疫毒性模型。染毒结束次日取脾脏组织,提取蛋白和RNA,Western-Blot检测Caspase-3、Caspase-8、Cyt-c、Bcl-2、Fas-l;RT-PCR检测Bid。结果脾脏细胞中Caspase-3/β-actin灰度比值各染毒组(0.322±0.030,0.374±0.024,0.482±0.032)均比对照组(0.254±0.039)增加(P<0.05)。24mg/(kg.d)染毒组Cyt-c/β-actin灰度比值(0.538±0.217)比对照组(0.206±0.046)增加(P<0.05)。各染毒组Bcl-2/β-actin灰度比值(2.440±0.050,1.998±0.094,1.512±0.094)均比对照组(2.921±0.067)低(P<0.05)。各染毒组促凋亡Bid基因表达(0.354±0.026,0.395±0.028,0.492±0.027)比对照组(0.322±0.032)增加(P<0.05)。结论交通相关的PM2.5可从线粒体途径诱导大鼠脾脏出现凋亡。
Objective To investigate the effect of traffic-related PM2.5 on apoptosis signal molecules in spleen of rats and provide experimental evidence for studying the immunotoxicity mechanism of traffic-related PM2.5. Methods The trachea was infused with different doses of [1.5mg / (kg · d), 6mg / (kg · d), 24mg / (kg · d · d)] Times, rat subacute immunotoxicity model was prepared. The spleen tissue was harvested on the next day after injection, protein and RNA were extracted, and Caspase-3, Caspase-8, Cyt-c, Bcl-2 and Fas-1 were detected by Western- Results The gray scale ratio of Caspase-3 / β-actin in spleen cells was significantly higher than that of the control group (0.322 ± 0.030,0.374 ± 0.024,0.482 ± 0.032) (P <0.05). The gray value of Cyt-c / β-actin (0.538 ± 0.217) in 24mg / (kg.d) exposure group was significantly higher than that in control group (0.206 ± 0.046) (P <0.05). The gray ratio of Bcl-2 / β-actin in each exposure group (2.440 ± 0.050, 1.998 ± 0.094, 1.512 ± 0.094) was lower than that in control group (2.921 ± 0.067) (P <0.05). Compared with control group (0.322 ± 0.032), the Bid gene expression in the treated groups increased (P <0.05). Conclusion Traffic-related PM2.5 induces apoptosis in rat spleen through mitochondrial pathway.