摘要
目的 :研究经饮水摄入微囊藻毒素 (MC)在大鼠肝癌发生期间对细胞增殖与凋亡的影响 ,进而探讨微囊藻毒素促肝癌机制。方法 :5 0只Wistar大鼠随机分为 4组 ,A组 (空白对照 ) :B组 (DEN启动对照 ) ;C组 (DEN处理 ,饮含MC藻水 ) :D组 (DEN处理 ,腹腔注射MCLR纯毒素 )、应用LSAB免疫组化技术检测大鼠肝癌前病变病灶中PCNA、Bcl 2和Bax蛋白的表达。结果 :各处理组PCNA平均积分光密度值 (AIOD)均较A组 0 .0 0 13明显升高 ,分别为B组 0 .0 0 33,C组 0 .0 0 36和D组 0 .0 0 88,其中D组与B组比较有明显升高 (P <0 .0 5 )。饮水摄入或腹腔注射微囊藻毒素均可使Bcl 2表达上调 ,Bax表达下调。结论 :促进调控细胞增殖与凋亡的基因平衡失调 .使细胞失控性生长 ,可能是微囊藻毒素促肝癌作用的分子机制之一。
Purpose: To study the effects of drinking water contaminated with microcystins(MC) on cell prolife \{ration\} and apoptosis during the course of hepatocarcinogenesis,and to probe the mechanism of promoting hepatocarcinogenesis of microcystic toxins. Methods: 50 healthy Wistar rats were randomly divided into 4 groups: group A (normal control); group B (treated with DEN only); group C (treated with DEN and MC contaminated water); group D (treated with DEN and microcystins i.p ). The PCNA, Bcl 2 and Bax protein expression in preneoplastic liver tissue were detected using immunohistochemical assays. Results: The average integrated optical densities (AIOD) of PCNA in the experimental groups were 0.0033(group B), 0.0036 ( group C ) and \{0.0088\} (group D) respectively, and they were all significantly increased as compared to group A (0.0013). But as comparing to group B, only group D had significantly higher PCNA expression. Up regulation of Bcl 2 and down regulation of Bax expression were found in group C and group D. Conclusion: Uncontrolled cell proliferation caused by unbalanced expression of Bcl 2 and Bax gene may be one of the mechanisms of hepatocarcinoma promoted by microcystins.
出处
《癌变·畸变·突变》
CAS
CSCD
2002年第4期214-217,共4页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
福建省科技项目 (项目号 :97Z176)
