Rubia cordifolia L.aqueous extractreduces visceral fat mass of high fat diet-induced obese rats
- VernacularTitle:茜草水溶性提取物减少高脂饮食诱导的肥胖大鼠内脏脂肪
- Author:
Kemin YAN
;
Jian XU
;
Huijuan ZHU
;
Hui PAN
;
Naishi LI
;
Linjie WANG
;
Hongbo YANG
;
Meijuan LIU
;
Fengying GONG
- Keywords:
Rubia cordifolia L.aqueous extract;
PPARγ2;
obesity;
visceral fat
- From:
Basic & Clinical Medicine
2017;37(9):1231-1236
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of a traditional Chinese medicine Rubia cordifolia L.aqueous extract (RCAE) on body weight, fat mass and parameters of glucose and lipid metabolism in high fat diet (HFD)-induced obese rats and its mechanism.Methods pGL3-Enhancer-PPARγ2 (625 bp)-Luc plasmid, a luciferase reportergene expression plasmid containing PPARγ2 promoter was constructed and stably transfected 3T3-L1 preadipocytes were established.PPARγ2 promoter`s activities in these cells were detected after administration with different concentration (0.1 mg/L~1 000 mg/L) of RCAE or with 100 mg/L RCAE for different action time.PPARγ2 mRNA expression in human adipocytes were detected after administration with 100 mg/L RCAE.Meanwhile, HFD-induced obese rats were administrated with low or high dose RCAE to investigate the effects of RCAE on serum glucose, lipid and insulin levels, body weight, visceral fat mass and so on.Results 10 mg/L RCAE could increase luciferase expression in 3T3-L1 cells to 1.43 folds of that in control group (P<0.01) and it reached 3.24 folds of that in control group when the concentration of RCAE was 1000 mg/L (P<0.01).With the administration with 100 mg/L RCAE, the luciferase activity of 3T3-L1 cells peaked at 28 h where it was 2.72 folds of that in control group (P<0.01), and the expression of PPARγ2 mRNA in human adipocytes increased to 2.27 folds of that in control group (P<0.01).Compared with HFD group, low dose RCAE significantly reduced the fasting insulin level, HOMA-IR and visceral fat mass (P<0.05).Conclusions Low dose RCAE significantly reduces the visceral fat mass and ameliorates insulin resistance in HFD-induced obese rats.The potential mechanism may be explained by the stimulation of PPARγ2 promoter activities and the increased expression of PPARγ2 gene.
