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目的探讨大黄素(emodin)对高脂喂养导致的非酒精性脂肪肝(NAFLD)大鼠脂质水平和肝脏脂质代谢基因表达的影响。方法大鼠高脂饮食6周形成NAFLD模型,大黄素低、高剂量(30、60 mg/kg)干预4周,肝脏HE染色观察NAFLD模型大鼠肝脏病理改变,检测血清和肝脏的甘油三酯(TG)、游离脂肪酸(FFA)和转氨酶(ALT、AST)水平;采用荧光实时定量PCR技术检测肝脏X受体(LXR)、固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合成酶(FAS)、二酰基甘油酰基转移酶2(DGAT-2)、硬脂酰辅酶A去饱和酶1(SCD-1)、脂酰辅酶A氧化酶(ACO)、肉毒碱棕榈酸转移酶-1(CPT-1)和过氧化物酶体增殖物激活受体α(PPAR-α)等脂质代谢基因表达。结果与模型组相比,大黄素低剂量组大鼠血清FFA、TG、ALT显著下降,肝脏HE染色显示脂质沉积减轻,SCD-1表达下降;高剂量组大鼠ALT、AST,血清和肝脏TG、FFA显著下降,肝脏脂质沉积显著下降,肝脏FAS、DGAT-2、SCD-1表达降低,CPT-1和PPAR-α的表达显著增高。结论大黄素剂量依赖性地改善NAFLD,其机制可能与下调肝脏脂质合成基因和上调脂肪酸氧化基因的表达有关。
Objective To investigate the effects of emodin on lipid levels and lipid metabolism gene expression in nonalcoholic fatty liver disease (NAFLD) rats induced by high fat diet. Methods The NAFLD model was induced by high-fat diet for 6 weeks in rats. Erythromycin was given to low and high doses (30, 60 mg / kg) for 4 weeks. HE staining was used to observe the pathological changes of hepatic tissue in NAFLD rats. Serum and liver triglyceride (TG), free fatty acids (FFA), and aminotransferases (ALT, AST) were detected by real-time PCR. Real-time quantitative PCR was used to detect the levels of liver X receptor (LXR), sterol regulatory element binding protein-1c (FAS), diacylglycerol acyltransferase 2 (DGAT-2), stearoyl-CoA desaturase 1 (SCD-1), acyl-CoA oxidase (ACO), carnitine palmitoyltransferase- 1 (CPT-1) and peroxisome proliferator-activated receptor α (PPAR-α) and other lipid metabolism gene expression. Results Compared with the model group, the levels of FFA, TG and ALT were significantly decreased in the emodin low-dose group. The hepatic HE staining showed that the lipid deposition was reduced and the expression of SCD-1 was decreased. The levels of ALT, AST, serum and liver TG, FFA decreased significantly, liver lipid deposition decreased significantly, liver FAS, DGAT-2, SCD-1 expression decreased, CPT-1 and PPAR-α expression was significantly increased. Conclusion Emodin can improve NAFLD in a dose-dependent manner, which may be related to the down-regulation of hepatic lipid synthesis genes and the up-regulation of fatty acid oxidation genes.