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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、My D88、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My D88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。
Objective To investigate the mechanism of emodin in improving hepatic lipid deposition in non-alcoholic fatty liver disease (NAFLD) rat model. Methods The rats were randomly divided into normal control group, NAFLD model group and emodin low, medium and high doses (20, 40, and 80 mg · kg -1), with 8 rats in each group. The model of NAFLD was induced by high fat diet. The pathological changes of liver were detected by HE staining. The contents of TNF-α and IL-1 in serum were detected by enzyme-linked immunosorbent assay. The expression of TLR4 signal was detected by real-time quantitative PCR and immunohistochemistry expression. Results Compared with the normal control group, the NAFLD group showed typical lipid droplet vacuoles of hepatocytes and mononuclear cells infiltration of some hepatocytes. The levels of serum TNF-α and IL-1 in the NAFLD group were significantly higher than those in the normal control group (P <0.05) , TRAF-6 gene expression increased (P <0.05). Compared with the NAFLD model group, the emodin groups significantly improved the lipid droplets vacuoles in the liver of NAFLD rats, inhibited the secretion of TNF-αand IL-1 (P <0.05), and inhibited the expression of TLR4 in the liver (P < 0.05). Emodin medium and high dose groups inhibited the expression of My D88 and TRAF-6 in the liver (P <0.05). Conclusion The mechanism of emodin in improving hepatic lipid deposition in NAFLD model is related to inhibiting TLR4 signal in liver.