复方贞术调脂方对非酒精性脂肪肝的肝PPARα及其下游基因的影响

发布时间：2018-10-24 19:38

【摘要】：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(P0.05),但是高脂喂养3个月后FTZ组小鼠体重明显低于模型组(P0.05)。治疗前,两组TG、TC及空腹血糖比较差异无统计学意义(P0.05)。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(P0.05),OGTT实验AUC明显减少(P0.05),肝脏中PPARα及CPT1 m RNA表达升高(P0.05,P0.01)。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(P0.05)。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。
[Abstract]:Objective to observe the preventive effect of compound Zhenzhu Tiaozhi recipe (FTZ) on non alcoholic fatty liver induced by high fat diet and to explore its related mechanism. Methods Twenty male C57BL/6j mice were randomly divided into model group and FTZ group with 10 mice in each group. Both groups were fed on a high-fat diet. The model group was given 5% Arabic gum solution and the FTZ group was given FTZ extract powder solution (1.17 g / kg daily, with 5% Arabic gum solution as solvent, 10 m L/kg), and the two groups were given the drug once a day. The drug was given for 5 months. The levels of blood glucose and blood lipid were measured before and after treatment. After treatment, oral glucose tolerance test (OGTT),) and area under curve area (AUC).) were calculated. The expression of peroxisome proliferator-activated receptor 伪 (PPAR 伪) and carnitine acyltransferase 1 (CPT1) m RNA) were detected by Real-time PCR. Results there was no significant difference in the amount of food intake between the two groups (P0.05), but the body weight of FTZ group was significantly lower than that of model group after 3 months of high-fat feeding (P0.05). Before treatment, there was no significant difference in TG,TC and fasting blood glucose between the two groups (P0.05). After treatment, compared with the model group, TC,TG, fasting blood glucose and liver TC,TG level in FTZ group were significantly decreased (P0.05), OGTT experimental AUC significantly decreased (P0.05), liver PPAR 伪 and CPT1 m RNA expression increased (P0.05 P0.01). There was no significant difference in liver weight, visceral fat and inguinal fat between the two groups (P0.05). In the model group, there was obvious lipid deposition in the liver, a large number of vacuolar degeneration and water-like degeneration of liver cells, lymphocyte infiltration and a small number of liver cell necrosis around the catchment area and the central vein. The degree of hepatic vacuolar degeneration and watery degeneration in FTZ group was significantly less than that in model group. Conclusion FTZ can delay the development of non-alcoholic fatty liver induced by high fat diet, and its mechanism is related to the up-regulation of liver PPAR 伪 and its downstream gene CPT1, to promote fatty acid oxidation and improve insulin sensitivity.
【作者单位】：广州中医药大学临床药理研究所;广东药科大学广东省代谢性疾病中医药防治重点实验室国家中医药管理局高脂血症调肝降脂重点研究室;
【基金】：国家自然科学基金资助项目(No.81173626) “新世纪优秀人才计划”(No.NECT-11-0916) 广东省自然基金团队项目(No.10351022401000000)
【分类号】：R285.5

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