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目的 研究亚急性微囊藻毒素染毒后 ,大鼠肝细胞凋亡及Bcl 2和p5 3基因在肝细胞凋亡过程中的作用 ,进而探讨微囊藻毒素肝毒性机制。方法 将SD大鼠随机分为 4组 ,每组雌雄各 10只 ,经 35d腹腔染毒后 ,剖杀、立即取肝脏 ,应用原位末端标记法观察亚急性染毒大鼠肝细胞凋亡 ,ABC免疫组化技术检测Bcl 2和P5 3蛋白表达。结果 发现在 4μg·kg-1·d-1剂量下 ,微囊藻毒素引起肝细胞凋亡与对照组相比无明显改变 ;但在 8μg·kg-1·d-1和 12 μg·kg-1·d-1的染毒剂量下 ,微囊藻毒素可明显引起大鼠肝细胞凋亡 ,凋亡率分别为 (2 90± 0 81) %和 (3 0 0± 0 40 ) % ;剂量 12 μg·kg-1·d-1时 ,肝细胞Bcl 2蛋白表达较对照组减弱 ;各染毒组P5 3蛋白的表达随着染毒剂量的增高较对照组增强。结论 微囊藻粗毒素在较低剂量下主要引起肝细胞凋亡 ,Bcl 2和p5 3基因在其引起凋亡的过程中可能起着一定的作用。
Objective To investigate the effect of subacute microcystin on apoptosis of hepatocytes and the role of Bcl-2 and p5 3 genes in hepatocyte apoptosis, and to explore the mechanism of microcystin-induced hepatotoxicity. Methods Sprague - Dawley rats were randomly divided into 4 groups with 10 in each group. After 35 days of intraperitoneal injection, the rats were sacrificed and the liver was taken immediately. The apoptosis of hepatocytes in subacutely exposed rats was observed by in situ terminal labeling. ABC immunohistochemical detection of Bcl 2 and P5 3 protein expression. The results showed that microcystin-induced hepatocyte apoptosis did not change significantly at the dose of 4μg · kg-1 · d-1 compared with that of the control group. However, at 8μg · kg-1 · d-1 and 12μg · kg- 1 · d-1, microcystin could obviously induce the apoptosis of hepatocytes in rats, the apoptotic rates were (2 90 ± 0 81)% and (300 ± 0 40)%, respectively 12 μg · kg-1 · d-1, the expression of Bcl2 protein in hepatocytes was weaker than that in control group. The expression of P53 protein increased with the increase of exposure dose. Conclusion The microtocytosis crude toxin mainly induces hepatocyte apoptosis at lower dose, and the Bcl-2 and p5 3 genes may play a role in the process of apoptosis.