人参皂苷Rg1对非酒精性脂肪肝病大鼠脂肪酸β-氧化的改善作用研究

Study on the improvement effect of Ginsenoside Rg1 on nonalcoholic fatty liver phenotype by regulation of β-oxidation

目的研究人参皂苷Rg1对非酒精性脂肪肝病(NAFLD)大鼠β-氧化的作用。方法将120只SD大鼠分为对照组(CON组)、模型组(HFD组)及人参皂苷Rg1低、中、高剂量组(GLD、GMD、GHD组)和熊去氧胆酸钠治疗组(PDT组),每组20只,分别于治疗4、8周后处死大鼠各半,肝脏切片HE染色,检测肝功能、血脂、肝脏脂酰CoA合成酶1(CoASH1)、脂酰肉毒碱转移酶I(CATI)及酰基辅酶A氧化酶1(ACOX1)mRNA和蛋白表达。结果治疗4周后,肝脏HE染色GHD组有改善,PDT、GLD、GHD组未见改善;8周后,PDT组与GLD组仍有少量脂肪颗粒聚集,GMD组和GHD组看不到任何脂滴浸润;治疗4周后,PDT、GLD、GMD、GHD组与HFD组相比,天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(AKP)、总胆固醇(TC)、三酰甘油(TG)及低密度脂蛋白胆固醇(LDL-C)明显降低(P<0.05),8周后进一步降低;治疗4周后,高密度脂蛋白胆固醇(HDL-C)4个组均升高,8周后几乎恢复到对照组的水平;治疗4周后肝脏组织CoASH1、CACTI及ACOX1表达4个组均显著升高(P<0.05),治疗8周后改善更为明显。结论人参皂苷Rg1可通过调节大鼠β-氧化来改善脂代谢及肝功能。

Objective To investigate the role of Ginsenosides Rg1 for non-alcoholic fatty liver disease byβ-oxidation.Methods 120 SD rats were randomly divided into control group（CON）,model group（HFD）,Ginsenosides Rg1 low,medium and high dose group（GLD,GMD and GHD）,sodium deoxycholate of bear treatment group（PDT）,20 rats in each group.After 4and 8weeks treatment,the rats were sacrificed,Pathology of hepatic tissue was tested by HE staining,and liver function,lipid levels,hepatic acyl-CoA synthetase（CoASH1）,carnitine acyl transferase I（CATI）and acetyl coenzyme A oxidase 1（ACOX1）mRNA and protein expression were tested.Results After 4weeks of treatment,the liver function tested by HE staining only improved in GHD group.After 8weeks,there＇s a little fat particles aggregation in PDT and GLD groups,but no infiltration of fat in GMD and GHD groups.After 4weeks,AST,ALT and AKP,CHOL,TG and LDL-C levels were significantly lower in PDT,GLD,GMD and GHD groups compared with HFD group（P〈0.05）,which were significant declined 8weeks later.After 4weeks,HDL-C level in four groups was significantly increased,then reached the normal level 8weeks later.After 4weeks,CoASH1,CATI and ACOX1 expressions in hepatic tissue of four groups were significantly increased,which improved more obviously after eight weeks.Conclusion Ginsenoside Rg1 can improves nonalcoholic fatty liver phenotype by regulation ofβ-oxidation.