小柴胡汤对高脂血症性模型大鼠的作用观察

[目的]探察小柴胡汤的降脂及抗脂肪肝形成的作用。[方法]SD大鼠连续给予脂肪乳剂灌胃造模后分成模型组、小柴胡汤小、大剂量组、辛伐他汀组,各组继续给予脂肪乳剂灌胃,其中小柴胡汤小、大剂量组予小柴胡汤中药灌胃,辛伐他丁组给予辛伐他丁溶液灌胃,观测各组大鼠血脂、肝重及肝HE的变化。[结果]模型组大鼠给予脂肪乳剂灌胃1w后,血脂较正常组显著升高(P<0.01或P<0.05),3w后血脂持续升高、肝脏指数增加及出现脂肪变。与模型组比较,各给药组大鼠血脂、肝脏指数及肝脂肪变程度均呈不同程度的降低,其中小柴胡汤大剂量组和辛伐他汀组的作用较明显。[结论]小柴胡汤具有一定的降脂及抗肝脂肪变的作用。

Hepatic steatosis:A benign disease or a silent killer

Steatosis is a common feature of many liver diseases,namely non-alcoholic steatohepatitis(NASH) and hepatitis C virus(HCV) infection,but the pathogenic mechanisms differ.Insulin resistance(IR),a key feature of metabolic syndrome,is crucial for NASH development,associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis.This may have potential implications for new drug therapy.In HCV-related disease,steatosis impacts both fibrosis progression and response to treatment.Steatosis in HCV-related disease relates to both viral factors(HCV genotype 3),and host factors(alcohol consumption,overweight,hyperlipidemia,diabetes).Among others,IR is a recognized factor.Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors.Thus,hepatic steatosis should not be considered a benign feature,but rather a silent killer.

Mixture of five herbal extracts ameliorates pioglitazone-induced aggravation of hepatic steatosis via activating the adiponectin receptor 2/AMP-activated protein kinase signal pathway in diabetic KKAy mice

OBJECTIVE: To assess the effect of a mixture of five herbal extracts(FT-5) on insulin resistance, glucose/lipid metabolism, hepatic steatosis, and to investigate whether the combination of FT-5 and pioglitazone would provide a robust effect on diabetes treatment, while may minimize undesirable side-effects of pioglitazone in diabetic Ay gene(KKAy)mice.METHODS: Seven-week-old KKAy mice were randomly divided into five groups: control(CON)group, FT-5(2.0 g/kg) group, pioglitazone(20 mg/kg)(PIO) group, pioglitazone(20 mg/kg) + FT-5(2.0 g/kg)(P + F) group. Age-matched C57 BL/6 J micewere used as the control group. After seven weeks of continuous intragastric administration of medication, the glucose metabolism, insulin sensitivity and lipid metabolism of KKAy mice were evaluated by assessing the fasting blood glucose(FBG), oral glucose tolerance test(OGTT), fasting serum insulin(FINS), insulin tolerance test(ITT), homeostasis model of assessment-insulin resistance index(HOMA-IR), total cholesterol(TC), total triglycerides(TG), and free fatty acids(FFA) in plasma and liver.Plasma and hepatic adiponectin were measured via enzyme-linked immunosorbent assays. Genes related to adipogenesis and lipolysis in white adipose tissues(WAT) and liver were examined by real-time polymerase chain reaction. Lipid metabolism-related protein expression in the liver of KKAy mice were detected by Western blotting.RESULTS: PIO treatment remarkably improved insulin resistance. However, it also showed substantial side effects. FT-5 group exhibited no significant decrease in serum glucose. However, it reduced fasting plasma TG levels and improved hepatic steatosis of KKAy mice. P + F group showed improved insulin resistance and similar body weight gain, as compared with control group. The m RNA expression of genes related to fatty acid oxidation was markedly up-regulated in the liver of P + F group.Pioglitazone administration markedly decreased the phosphorylation levels of AMPK, as compared with all other groups. Besides, even though plasma adiponectin increased in PIO, FT-5, P + F group, adipo R2 gene expression significantly decreased in the liver of PIO group.CONCLUSION: FT-5 decreased plasma TG and alleviated aggravating hepatic steatosis induced by pioglitazone in KKAy mice. FT-5's mechanism might be associated with its ability to activate the Adipo R2/AMPK pathway.