Objective:To determine the effects of ginsenoside rg3 on the body weight of C57BL/6J obese mice and to investigate its underlying weight loss mechanisms with a focus on white fat browning-related factors.Methods:Eight-week-old C57BL/6J male mice were fed a high-fat diet for 12 successive weeks to construct the obese model.C57BL/6J male mice were fed a standard chow diet to construct normal control group.After 8 weeks of intervention with ginsenoside rg3,the food intake,body weight,body fat mass,blood sugar,and lipid profiles of the mice in each group were detected.Hematoxylin and eosin(HE)staining was used to observe the histological morphology of the adipose tissues.Real-time polymerase chain reaction(RT-PCR)and Western blotting(WB)were applied to detect the gene and protein expression levels of peroxisome proliferators-activated receptor gama(PPARg),Peroxisome proliferatoractivated receptor-gamma coactivator-1alpha(PGC-1a),PR domain containing 16(PRDM16),and uncoupling protein 1(UCP-1).Results:Compared to normal control group mice,the body weight,food intake,body fat composition,and blood lipid levels of model group mice increased significantly.After 8 weeks of intervention with ginsenoside rg3,body weight,body fat composition,food intake,and blood lipid profiles decreased.HE staining showed that ginsenoside rg3 can improve white adipocyte hypertrophy to a certain extent.RTPCR and WB demonstrated that ginsenoside rg3 can increase the mRNA and protein expression levels of PPARg,PGC-1a,PRDM16,and UCP-1 in the adipose tissues of obese mice.Conclusion:The weight reduction effect of ginsenoside rg3 may be related to the promotion of white fat browning.
目的:探讨降糖消渴颗粒对高脂饮食诱导自发性2型糖尿病KKAy小鼠肾脏c-Jun氨基末端激酶(JNK)信号通路。方法:将40只成模的KKAy小鼠按血糖、体质量随机分为模型组,吡格列酮组,中药高、中、低剂量组(每日分别以降糖消渴颗粒7.0、3.5、1.75g/kg体质量灌胃),每组8只,另设8只C57BL/6J小鼠为正常组。模型组和正常组给予蒸馏水,其余组给予对应量的药液灌胃。干预10周后,检测各组小鼠空腹血糖(FBG)、血清尿素氮(BUN)、肌酐(Scr)、白蛋白(ALB)、总蛋白(TP)的含量,用RT-PCR检测肾组织JNK m RNA的表达,Western Blot检测各组小鼠JNK1、JNK2、P-JNK蛋白的表达情况,HE染色观察药物对糖尿病小鼠肾脏病理改变的影响。结果:与正常组小鼠比较,模型组小鼠FBG、BUN与Scr水平显著上升(P<0.05),ALB、TP水平明显下降(P<0.05),而JNK m RNA及JNK1、JNK2、P-JNK蛋白表达明显上调;药物干预10周后能够显著降低FBG、BUN与Scr水平,升高ALB、TP水平,与模型组比较差异具有统计学意义(P<0.01,P<0.05);各给药组较模型组的JNK m RNA及JNK1、JNK2、P-JNK蛋白表达则表现出下调的趋势(P<0.01,P<0.05);HE染色显示降糖消渴颗粒对肾脏病理改变有一定的保护作用。结论:降糖消渴颗粒对糖尿病小鼠肾损伤有一定的保护作用,其作用机制可能与抑制JNK信号通路激活有关。
Objective:To determine the effect of Salvianolic acid B (Sal B) on glucose and lipid metabolism in mice with high-fat diet (HFD)-induced obesity,and to investigate the underlying mechanisms by measuring the expression levels of key adipogenic transcription factors.Methods:Six-week-old C57BL/6J male mice were fed for 12 weeks with a HFD to induce obesity or a standard diet to serve as normal controls.A mean body weight increase of more than 20% after these 12 weeks was used as the criteria for obesity.HFD-fed obese mice then received a supplement of Sal B (100 mg/kg body weight/day),metformin (75 mg/kg body weight/day) or water (an equivalent volume;served as model controls) by oral gavage for an additional 8 weeks,and the normal controls received water (an equivalent volume) by oral gavage for the same period.Results:Sal B significantly reduced body weight gain (P <.05) without influencing food intake in HFD-fed obese mice relative to model controls.Sal B also reduced the body fat mass of the obese mice relative to model controls in a time-dependent manner (P <.05).Sal B significantly decreased the serum concentrations of low-density lipoprotein cholesterol,total cholesterol,triglyceride and free fatty acids by 25.5%,20.2%,20.6% and 13.4%,respectively,and increased the concentration of high-density lipoprotein cholesterol by 50.1% relative to model controls.In addition,Sal B significantly lowered fasting glucose concentrations and improved insulin sensitivity relative to model controls (P <.05).Sal B acted by ameliorating the histopathological changes in both brown and white adipose tissues of obese mice.Moreover,in brown adipose tissue,Sal B up-regulated the mRNA and protein expression of PPARγ and c/EBPα,and the protein expression of PPARα and SREBP-1 (P <.05).In white adipose tissue,Sal B down-regulated the mRNA expression of PPARγ and c/EBPα,and decreased the protein expression of PPARγ and SREBP-1(P <.05).Conclusjons:The results suggest that Sal B can reduce body weight gain and regulate glucose and li
