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目的观察复方贞术调脂方(FTZ)对高脂饮食致非酒精性脂肪肝的预防作用,并探讨其相关机制。方法 20只雄性C57BL/6j小鼠按随机数表法分为模型组及FTZ组,每组10只。两组均予高脂饮食喂养,同时模型组予5%阿拉伯树胶水溶液灌胃,FTZ组予FTZ浸膏粉溶液灌胃(每日1.17 g/kg,以5%阿拉伯树胶水溶液为溶剂,10 m L/kg灌胃给药),两组每日1次给药,共给药5个月。监测小鼠进食量及体重情况,检测治疗前后小鼠血糖、血脂水平,治疗后进行口服糖耐量实验(OGTT),并计算曲线下面积(AUC)。观察肝脏病理情况,测定肝脏脂质含量,Real-time PCR法检测肝内过氧化物酶体增殖物激活受体α(PPARα)、肉碱脂酰转移酶1(CPT1)m RNA表达。结果两组小鼠进食量相近,差异无统计学意义(P>0.05),但是高脂喂养3个月后FTZ组小鼠体重明显低于模型组(P<0.05)。治疗前,两组TG、TC及空腹血糖比较差异无统计学意义(P>0.05)。治疗后,与模型组比较,FTZ组小鼠TC、TG、空腹血糖、肝脏TC、TG水平降低(P<0.05),OGTT实验AUC明显减少(P<0.05),肝脏中PPARα及CPT1 m RNA表达升高(P<0.05,P<0.01)。两组小鼠肝脏重量、内脏脂肪及腹股沟脂肪称重结果比较,差异无统计学意义(P>0.05)。模型组小鼠可观察到肝脏明显脂质沉积,汇管区周围、中央静脉周围可见大量肝细胞空泡变性及水样变性,淋巴细胞浸润,少量肝细胞点状坏死。而FTZ组肝脏空泡变性及水样变性程度明显轻于模型组。结论 FTZ可延缓高脂饮食所致的非酒精性脂肪肝的发生,其机制与上调肝PPARα及其下游基因CPT1,促进脂肪酸氧化,改善胰岛素敏感性有关。
Objective To observe the preventive effect of Fufang Zhenzhu Tiaozhi Recipe (FTZ) on non-alcoholic fatty liver caused by high-fat diet and to explore its mechanism. Methods Twenty male C57BL / 6j mice were randomly divided into model group and FTZ group according to random number table. Both groups were fed with high-fat diet, while the model group was treated with 5% Gum arabic solution. FTZ group was given FTZ extract powder solution (1.17 g / kg daily, 5% gum arabic solution as solvent, 10 m L / kg gavage), two groups once daily dosing for a total of 5 months. The food intake and body weight of mice were monitored. Blood glucose and blood lipid levels were measured before and after treatment. Oral glucose tolerance test (OGTT) was performed after treatment, and the area under the curve (AUC) was calculated. The pathological changes of the liver were observed. The content of liver lipid was measured. The expression of peroxisome proliferator - activated receptor α (PPARα) and carnitine acyltransferase 1 (CPT1) m RNA in the liver were detected by Real - time PCR. Results There was no significant difference in food intake between the two groups (P> 0.05). However, the body weight of FTZ group was significantly lower than that of the model group (P <0.05) after 3 months of high-fat diet. Before treatment, there was no significant difference in TG, TC and fasting blood glucose between the two groups (P> 0.05). After treatment, the levels of TC, TG, fasting blood glucose, liver TC and TG in FTZ group were significantly lower than those in the model group (P <0.05), and the AUC in OGTT group was significantly decreased (P <0.05). The expression of PPARα and CPT1 mRNA (P <0.05, P <0.01). There was no significant difference in liver weight, visceral fat and inguinal fat weight between the two groups (P> 0.05). In the model group, significant lipid deposition was observed in the liver. A large number of hepatocytes were found around the portal area and around the central veins. Degeneration and watery degeneration, lymphocytic infiltration and a small amount of punctate necrosis of hepatocytes were observed. However, the extent of hepatic vacuolar degeneration and watery degeneration in FTZ group was significantly lighter than that in model group. Conclusion FTZ can delay the non-alcoholic fatty liver disease induced by high-fat diet. The mechanism is related to up-regulating hepatic PPARα and its downstream gene CPT1, promoting fatty acid oxidation and improving insulin sensitivity.