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目的 探讨微囊藻毒素 (MC)促肝癌的分子机制。方法 采用二阶段致癌理论建立中期试验动物模型 ,γ 谷氨酰转肽酶 (γ GT)染色检验MC的促癌作用 ,并以免疫组化法结合图像分析技术精确测定大鼠肝脏bcl 2和bax基因的表达情况。结果 MC在促大鼠肝癌过程中能显著增加γ GT阳性率 ,γ GT染色的阳性率纯毒素组为 1 0 0 % ,显著高于二乙基亚硝胺 (DEN)对照组的 2 2 2 2 %。MC在促大鼠肝癌过程中能显著降低大鼠肝脏bax基因的表达强度和面积 ,bax表达的强度和面积纯毒素组分别为 0 0 2 83和 0 0 0 73 ,显著高于强度和面积分别为 0 0 65 5和 0 0 2 4 4的DEN对照组。MC在促大鼠肝癌过程中能显著增加大鼠肝脏bcl 2基因表达强度和面积 ,bcl 2表达的强度和面积纯毒素组分别为 0 0 977和 0 0 31 5 ,显著高于强度和面积分别为 0 0 4 6 0和 0 0 2 0 5的DEN对照组。结论 进一步证明了MC具有促肝癌作用。调节与细胞凋亡相关的癌基因和抑癌基因表达可能是MC促癌过程的重要机制之一。
Objective To investigate the molecular mechanism of microcystin (MC) promoting liver cancer. Methods The second-stage carcinogenesis theory was used to establish a mid-term experimental animal model. Γ-GT was used to test the carcinogenic effect of MC. The expressions of bcl-2 and bax in rat liver were determined by immunohistochemistry and image analysis Gene expression. Results MC could significantly increase the positive rate of γ-GT in rats with hepatocellular carcinoma. The positive rate of γ GT staining was 100% in pure toxin group, which was significantly higher than that in control group of diethylnitrosamine (DEN) group 2 %. MC in rat liver cancer can significantly reduce rat liver bax gene expression intensity and area, the intensity and area of bax expression of pure pox were 0 0 2 83 and 0 0 0 73, significantly higher than the intensity and area respectively DEN control group with 0 0 65 5 and 0 0 2 4 4. MC in rat liver cancer can significantly increase the rat liver bcl 2 gene expression intensity and area, the intensity and area of bcl 2 expression of pure toxins were 0 0 977 and 0 0 31 5, significantly higher than the intensity and area respectively DEN control group of 0 0 4 6 0 and 0 0 2 0 5. Conclusions further proved that MC has the role of promoting liver cancer. Regulating apoptosis-related oncogenes and tumor suppressor gene expression may be one of the important mechanisms of MC promoting cancer process.