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目的:探讨氯化甲基汞(MMC)中毒大鼠小脑变性的病理改变及机制。方法:本研究在大鼠服用MMC4mg/(kg·d)所致的亚急性汞中毒模型上,分别在服用MMC后第11、15、18和21天断头,采用组织和免疫病理技术动态观察小脑的病理演变,并采用TUNEL染色观察细胞凋亡改变,同时在电镜下观察了超微结构改变。结果:在服用MMC第18天,TUNEL染色显示小脑颗粒细胞有散在的凋亡细胞,主要位于脑回深部近白质区的颗粒层。第21天,凋亡细胞明显增加,颗粒细胞减少。MRF-1染色可见大量的小胶质细胞反应,GFAP示胶质细胞增生明显,而Purkinje细胞则保留完整。服用MMC第18天的超微结构观察表明,细胞核皱缩,体积缩小,形态不规则,电子密度增高,可见密集深染的染色质,部分细胞核破碎,呈现为均一深染的泪珠状染色质,符合凋亡改变。结论:本研究结果表明汞中毒的小脑变性的病理机制为细胞凋亡,其病理变化符合人类汞中毒表现。
Objective: To investigate the pathological changes and mechanism of cerebellar degeneration induced by methylmercury chloride (MMC) in rats. Methods: The rats were subcutaneously injected with MMC (4 mg / (kg · d)) on the 11th, 15th, 18th and 21st day after MMC administration. The animals were sacrificed on days 11, 15, 18 and 21, respectively. The tissue and immunohistochemistry The pathological changes of cerebellum were observed. TUNEL staining was used to observe the changes of apoptosis. Ultrastructural changes were also observed under electron microscope. RESULTS: On the 18th day after taking MMC, TUNEL staining showed scattered apoptotic cells in cerebellar granule cells, mainly located in the granular layer near the white matter area in the deep brain. On the 21st day, the apoptotic cells increased obviously and the granular cells decreased. A large number of microglial responses were observed in MRF-1 staining. GFAP showed glial proliferation significantly, while Purkinje cells remained intact. Microscopic observation on the 18th day of taking MMC showed that the nucleus was shrinking, the volume was reduced, the shape was irregular, the electron density was increased, densely stained chromatin was observed, part of the nucleus was broken, and the stained teardrop- In line with the change of apoptosis. Conclusion: The results of this study indicate that the pathological mechanism of cerebellar degeneration of mercury poisoning is apoptosis, and its pathological changes are in line with the performance of human mercury poisoning.