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目的从“脂联素-游离脂肪酸代谢”路径,探讨祛湿化瘀方对实验性脂肪肝游离脂肪酸抑制作用的机理。方法运用单纯高脂饮食诱导大鼠脂肪肝模型,自造模第7周起,21只大鼠被随机分为模型组和祛湿化瘀方高、低剂量组,每组7只,灌胃饮用水或给药4周。观察肝组织游离脂肪酸(FFA)、甘油三酯(TG)、肝脂肪变性程度、血清脂联素(ADP)、肝组织脂联素受体(AdipoR2)、腺苷酸活化的蛋白激酶(AMPK)、脂肪酸合成酶(FAS)、乙酰辅酶A羧化酶(ACCase)、丙二酰辅酶A(Malonyl-CoA)含量的变化,并与正常组进行对照。结果与模型组比较,祛湿化瘀方高、低剂量组的肝组织TG、FFA含量、FAS、ACCase和Malonyl-CoA显著降低(P<0.01或P<0.05),而AdipoR2、AMPK、血清ADP含量显著升高,并呈量效关系(P<0.05或P<0.01)。结论祛湿化瘀方对“脂联素-游离脂肪酸代谢”路径有显著的干预效应,其对脂联素及其受体的作用是该方降低肝组织FFA从而减轻肝脏脂质沉积的重要机理之一。
Objective To investigate the mechanism of Qushi Huayu Recipe inhibiting experimental fatty liver fatty acid from the path of “adiponectin - free fatty acid metabolism”. Methods Fatty liver rats were induced by simple high fat diet. From the 7th week after the model was established, 21 rats were randomly divided into model group and high and low dose Qushi Huayu Fang group, with 7 rats in each group. Drink or drink for 4 weeks. The levels of free fatty acid (FFA), triglyceride (TG), degree of hepatic steatosis, serum adiponectin (ADP), hepatic adiponectin receptor (AdipoR2), adenylate activated protein kinase , Fatty acid synthase (FAS), acetyl coenzyme A carboxylase (ACCase) and malonyl-CoA were measured and compared with the normal group. Results Compared with the model group, the contents of TG, FFA, FAS, ACCase and Malonyl-CoA in liver tissue of QFH group and low dose group were significantly decreased (P <0.01 or P <0.05), while AdipoR2, Content was significantly increased, and the dose-effect relationship (P <0.05 or P <0.01). Conclusion Qushi Huayu Recipe has a significant intervention effect on the pathways of adiponectin-free fatty acid metabolism. Its effect on adiponectin and its receptor is that it reduces the hepatic FFA and thus reduces the hepatic lipid deposition One of the important mechanisms.