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目的 探讨大鼠汞中毒时小脑颗粒层细胞凋亡与半胱氨酸蛋白酶 (caspases) 3及Bcl 2的关系。方法 在大鼠服用氯化甲基汞 (MMC) 4mg/kg每日 1次的动物汞中毒模型上 ,观察汞中毒第 11、15、18、19d大鼠的组织及免疫病理改变 ,并采用激光微分离术结合逆转录聚合酶链反应 (RT PCR) ,观察了颗粒层细胞凋亡与caspases 3及Bcl 2的关系。结果 汞中毒 18d组 ,大鼠小脑脑回深部近白质区的颗粒层出现TUNEL染色阳性的凋亡细胞 ;汞中毒 19d组 ,凋亡细胞的数量明显增加 ,颗粒层细胞破坏 ,但Calvidine染色显示Purkinje细胞的结构及形态正常。MRF 1及GFAP染色可见大量的小胶质细胞反应及星形细胞增生。汞中毒第 11d开始 ,与凋亡密切相关的因子caspases 3mRNA的表达开始上调 ,并逐渐增加 ,至 18d时达到高峰 ,但第 19d时明显下降。主要的抗凋亡因子Bcl 2则呈现相反的变化 ,在中毒后第 11d表达下调 ,第 19d时尤为明显 ,颗粒细胞的标志物Zic 1在汞中毒后即逐渐下降 ,提示颗粒细胞破坏。结论 汞中毒导致的小脑颗粒层细胞变性与caspases 3介导的细胞凋亡及Bcl 2下调有关。
Objective To investigate the relationship between cerebellar granular layer apoptosis and caspases 3 and Bcl 2 in rats with mercury poisoning. Methods Histological and immunological pathological changes of rats on the 11th, 15th, 18th and 19th day after mercury poisoning were observed on a model of mercury poisoning in rats treated with methylmercury chloride (MMC) 4mg / kg once a day. Microdissection combined with reverse transcription polymerase chain reaction (RT PCR) was used to observe the relationship between granulosa cell apoptosis and caspases 3 and Bcl 2. Results Mercury poisoning 18d group, TUNEL-positive apoptotic cells appeared in the granular layer of the white matter in the deep part of cerebellum of cerebellum. Mercury poisoning 19d group, the number of apoptotic cells increased significantly, granulosa cells destroyed, but Calvidine staining showed Purkinje The structure and morphology of cells is normal. MRF 1 and GFAP staining showed a large number of microglial responses and astrocytosis. At the 11th day after mercury poisoning, the expression of caspases 3 mRNA, a factor closely related to apoptosis, began to increase and gradually increased, reaching a peak at 18 days, but decreased significantly at the 19th day. The main anti-apoptotic factor Bcl 2 showed the opposite change, which was down-regulated on the 11th day after poisoning, especially on the 19th day. The Zic 1, a marker of granulosa cells, decreased gradually after mercury poisoning, suggesting that the granulosa cells destroyed. Conclusions The degeneration of cerebellar granule layer caused by mercury poisoning is related to the caspases 3 -mediated apoptosis and the down-regulation of Bcl 2.