中文摘要：

目的探讨大黄素改善非酒精性脂肪肝（NAFLD）大鼠模型肝脏脂质沉积的机制。方法大鼠随机分为正常对照组,NAFLD模型组,大黄素低、中、高（20,40,80 mg·kg^（-1））剂量组,每组8只。采用高脂诱导的方法建立NAFLD大鼠模型,采用HE染色法检测肝脏病理变化,酶联免疫法检测血清TNF-α、IL-1含量,实时定量PCR法和免疫组化染色法检测TLR4信号的表达。结果 NAFLD组大鼠呈现典型的肝细胞脂滴空泡,部分肝细胞有单核细胞浸润,与正常对照组比较,血清TNF-α、IL-1增高（P〈0.05）,肝脏TLR4、MyD88、TRAF-6的基因表达增高（P〈0.05）。与NAFLD模型组比较,大黄素各剂量组对NAFLD大鼠肝脏脂滴空泡均有显著改善,抑制血清TNF-α、IL-1分泌（P〈0.05）,并抑制肝脏TLR4的表达（P〈0.05）,大黄素中、高剂量组抑制肝脏MyD88和TRAF-6的表达（P〈0.05）。结论大黄素改善NAFLD模型肝脏脂质沉积的机制与抑制肝脏TLR4信号有关。

英文摘要：

Objective To explore the mechanism of emodin in improving hepatic lipid deposition of non- alcoholic fatty liver disease（NAFLD）model. Methods NAFLD rat model was established by high fat feeding. NAFLD rats were given oral administration of emodin 20, 40, 80 mg/kg for 2 weeks. HE staining was used for detecting hepatic pathology,ELISA was used for the detection of serum tumor necrosis factor alpha（TNF- α） and interleukin- 1（IL- 1）,and real time PCR and immunohistochemical staining were used to detect the expression of TLR4 signaling. Results The HE pathological slice showed that the liver of NAFLD rat had typical hepatic steatosis, and some hepatocytes were infiltrated by monocytes. The levels of serum TNF- α and IL- 1 were increased, the difference being significant.Compared with the normal control group, hepatic TLR4, My D88, TRAF6 expression levels of NAFLD group were increased significantly（P〈0.05）. Compared with NAFLD group,the hepatic steatosis of emodin groups was relieved,the serum TNF- α and IL^（-1）levels were decreased significantly（P〈0.05）,and hepatic TLR4 expression were downregulated significantly（P〈0.05）. Compared with NAFLD group,hepatic My D88 and TRAF- 6 expression of middleand high- dose emodin groups were decreased significantly（P〈0.05）. Conclusion The anti- NAFLD effect of emodin has a close relation with the inhibition of hepatic TLR4 signaling expression.