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首页> 外文期刊>Chinese journal of digestive diseases >Effect of proapoptosis protein on hepatocarcinogenesis.
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Effect of proapoptosis protein on hepatocarcinogenesis.

机译：促凋亡蛋白对肝癌发生的作用。

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摘要

OBJECTIVE: The goal of the present study was to determine how proapoptosis proteins regulate the progression of liver proliferative foci and tumorigenesis initiated by a chemical carcinogen, diethylnitrosamine (DEN). METHODS: Bid-deficient mice (15-day-old) were injected with 15 microg/g of DEN, then killed at 3 and 10 days, and 4 and 8 months after injection for analysis of hepatocellular proliferation, apoptosis and tumorigenesis. RESULT: The rate of apoptosis in the hepatocytes of the wild-type mice was significantly higher than in the Bid-deficient mice at 10 days after DEN exposure (P < 0.0001); the results of BrdU labeling agreed with the measurement of apoptosis in these animals, showing an obvious increase in the wild-type mice compared with the Bid-deficient mice (P < 0.0001). Four months after DEN exposure, the number and size of lesion foci or nodules in the wild-type mice were both greater than in the Bid-deficient mice (P < 0.05 and P < 0.001, respectively), but there was no significant difference between the two groups of mice at 8 months. CONCLUSION: These results suggest that a lack of apoptosis in liver tissue in the early stage after DEN exposure decreased some of the tumorigenesis potential of DEN.
机译：目的：本研究的目的是确定凋亡蛋白如何调节由化学致癌物二乙基亚硝胺（DEN）引发的肝增殖灶和肿瘤发生的过程。方法：对15日龄的缺乏出价的小鼠注射15微克/克的DEN，然后在注射后3、10天和4、8个月处死，以分析肝细胞增殖，凋亡和肿瘤发生。结果：DEN暴露后10天，野生型小鼠肝细胞凋亡率明显高于Bid缺乏型小鼠（P <0.0001）。 BrdU标记的结果与这些动物的细胞凋亡测量结果相符，与Bid缺陷小鼠相比，野生型小鼠明显增加（P <0.0001）。 DEN暴露后四个月，野生型小鼠的病灶或结节的数量和大小均大于Bid缺陷小鼠（分别为P <0.05和P <0.001），但两者之间无显着差异。两组小鼠在8个月时。结论：这些结果表明，DEN暴露后早期肝组织中缺乏细胞凋亡降低了DEN的某些致瘤潜力。

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