中文摘要：

目的研究内质网应激相关因子及其介导的凋亡途径在酒精性脂肪性肝病大鼠发病过程中的变化及意义。方法Wistar大鼠40只随机分为正常组（8只）、模型组（酒精混合液喂养）；模型组又分为4、8、12、16周4个时相点（各8只）；采集标本后检测血清生化指标，观察肝脏病理组织学改变，对肝脏脂肪变程度和炎症活动度评分及肝组织中GRP78、SREBPl-C、Caspase．3蛋白表达及动态变化。结果与正常组比较，模型组大鼠第8周时肝组织中GRP78、SREBPl-C、Caspase-3蛋白表达开始升高，于16周时达最强，差异有显著统计学意义（P〈0．01）。结论由GRP78、SREBPl-C、Caspase-3等相关调控因子介导的肝细胞内质网应激和凋亡反应途径参与了酒精性脂肪性肝病大鼠肝脏脂肪变性和炎症反应，并与酒精性脂肪性肝病发病机制关系密切。

英文摘要：

Objective To study the change and significance of endoplasmic reticulum stress related factors induced apoptosis way in alcoholic liver disease （ALD） process in rats. Methods 40 Wistar rats randomly divided into normal group （8） and the model group （fed with alcohol mixture）. The model group was divided into 4 sub-groups of 8 rats in each by different points of time 4,8,12,16 weeks; the changes of serum biochemical indices, the pathological and histo- logical character, the scores of hepatic steatosis degree and inflammation activity and the protein expression levels of GRP78,SREBP-le,Caspase-3 in liver tissue were observed. Results Compared with the normal group, the protein ex- pressions of GRP78, SREBPI-c, Caspase-3 in 8th week were significantly increased and these peak was reached in 16th week in model group （P 〈0. 01）. Conclusion The endoplasmic reticulum stress of liver cells mediated by GRP78, SREBPI-c, Caspase-3 related control factors and apoptosis reaction approaches are involved in alcoholic fatty liver disease rat hepatic steatosis and inflammation, and they are closely related with ALD pathogenesis.