摘要
目的探讨肝细胞凋亡及凋亡相关基因Caspase-3、Bcl-2在慢性乙型重型肝炎(慢重肝)发生发展机制中的作用。方法选择慢重肝肝组织标本68例(慢重肝组),正常肝组织标本20例(对照组)。采用原位末端转移酶标记技术(terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling,TUNEL)技术和免疫组织化学法检测2组肝组织中Cas-pase-3和Bcl-2的表达及肝细胞凋亡情况。结果慢重肝组凋亡指数的平均值为41.6±4.9,而在正常对照组肝组织中,未见到TUNEL阳性表达的肝细胞,2组差异有统计学意义。慢重肝组的肝组织中Caspase-3蛋白阳性表达程度明显高于对照组(P<0.05),而Bcl-2蛋白阳性表达程度明显低于对照组。Spearman相关分析发现,慢重肝组的肝组织中肝细胞凋亡指数与Caspase-3表达之间呈正相关(r=0.592,P<0.01),与Bcl-2表达之间呈负相关(r=-0.461,P<0.05)。结论肝细胞凋亡在慢重肝的发生过程中起重要作用,而Caspase-3和Bcl-2均参与了慢重肝的肝细胞凋亡过程。
Objective To investigate the role of hepatocyte apoptosis and apoptosis-related genes Caspase-3 and Bcl-2 in the pathogenesis of chronic severe hepatitis B. Methods Samples of liver tissues from 68 patients with chronic severe hepatitis B and 20 healthy controls were detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL） assay and immunohistochemical staining in order to observe the expression of Caspase-3 and Bcl-2 and hepatocyte apoptosis. Results The mean apoptotie index （AI） in chronic severe hepatitis B group was 41.6±4.9, while in the control group no positive expression of hepatocytes was detected by TUNEL assay. The difference between the two groups was statistically significant （P〈0.01）. Positive expression of Caspase-3 in chronic severe hepatitis B group was significantly higher than that in the control group （P〈0.05）, while that of Bcl-2 in chronic severe hepatitis B group was significantly lower than that in the control group （P〈0.05）. According to Spearman analysis, there was a positive correlation between AI and the expression of Caspase-3 （r=0.592, P〈0.01）, and a negative correlation between AI and the expression of Bcl-2 （r=-0.461, P〈0.05） in the chronic severe hepatitis B group. Conclusions Hepatocyte apoptosis may play a significant role in the pathogenesis of chronic severe hepatitis B. Caspase-3 and Bcl-2 participate in the hepatocyte apoptosis of chronic severe hepatitis B.
出处
《传染病信息》
2011年第4期221-223,共3页
Infectious Disease Information
基金
国家"十一五"科技重大专项(2008ZX10002-005-6)
