摘要
目的:探讨凋亡调控蛋白Bcl-2、Bax表达在大鼠非酒精性脂肪性肝病(NAFLD)中的作用.方法:采用高脂饮食建立大鼠NAFLD模型,以正常饮食设立对照组.HE染色观察肝脏脂肪变、炎症活动和纤维化程度,采用Western blot检测Bcl-2、Bax在肝脏组织中的表达.结果:实验组大鼠4wk可见轻度脂肪变,8wk呈单纯性脂肪肝改变,至12wk肝小叶内肝细胞弥漫性脂肪变,伴大量炎性细胞浸润,个别出现肝纤维化.Western blot结果显示,实验组大鼠4、8、12wk肝组织Bax蛋白表达显著高于对照组(0.61±0.03,0.78±0.03,1.02±0.03vs0.51±0.03,均P<0.01),Bcl-2蛋白随着造模时间的延长,表达逐渐下降(0.39±0.01,0.28±0.01,0.15±0.01vs0.52±0.01,均P<0.01),Bcl-2、Bax两者比率逐渐降低,尤以12wk降低明显.结论:在NAFLD发生过程中,细胞凋亡调节蛋白Bax表达上调,Bcl-2表达减少,二者表达的相对比例发生异常.这可能是NAFLD中肝细胞发生凋亡的重要原因之一.
AIM：To investigate the role of apoptosisregulated proteins Bcl-2 and Bax in the progression of nonalcoholic fatty liver disease （NAFLD）in rats. METHODS：An experimental rat model of NAFLD was established by feeding rats a fatrich diet（NAFLD group）.Control animals were fed a standard diet（control group）.Hepatic steatosis,inflammation and fibrosis were graded by routine HE staining of liver sections.The expression levels of Bcl-2 and Bax proteins in the liver were determined by Western blot. RESULTS：The NAFLD model rats exhibited mild steatosis at week 4,simple fatty liver at week 8,and severe steatohepatitis with fibrosis at week 12.Western blot analysis showed that hepatic expression of Bax protein in the NAFLD group was more pronounced from week 4,and continued to rise at weeks 8 and 12 when compared with the control group（0.61±0.03,0.78± 0.03 and 1.02±0.03 vs 0.51±0.03,respectively; all P〈0.01）,while the expression of Bcl-2 de-creased with the progression of fatty liver（0.39 ±0.01,0.28±0.01 and 0.15±0.01 vs 0.52±0.01, respectively;all P〈0.01）.Bcl-2/Bax ratio in the NAFLD group decreased in a time-dependent manner,particularly prominent at week 12. CONCLUSION：NAFLD may cause increased hepatic expression of Bax but decreased expression of Bcl-2,and the decrease in Bcl-2/Bax ratio may accelerate hepatocyte apoptosis.
出处
《世界华人消化杂志》
CAS
北大核心
2009年第23期2409-2412,共4页
World Chinese Journal of Digestology
