Chen Ching-Chu, Hsiang Chien-Yun, Chiang An-Na, Lo Hsin-Yi, Li Chia-Ing
Division of Endocrinology and Metabolism, Department of Medicine, China Medical University Hospital, Taiwan.
J Ethnopharmacol. 2008 Jun 19;118(1):46-50. doi: 10.1016/j.jep.2008.03.001. Epub 2008 Mar 13.
The molecular mechanism of a traditional hypoglycemic Chinese herbal formula.
To explore the glucose uptake effect as well as the mechanism(s) of action of Bai-Hu-Tang (BHT), a traditional Chinese herbal formula, composed of anemarrhena, gypsum, licorice and rice.
Differentiated 3T3-L1 adipocytes were treated with vehicle, insulin or insulin plus different concentrations of BHT. The 2-deoxy-[(3)H] glucose uptake assay was performed to measure the amount of glucose uptake. To explore the mechanism(s) of glucose uptake of BHT, we used two insulin signaling transduction inhibitors, N-Acetyl-Leu-Leu-Norleu-al (ALLN), a calpain inhibitor, and LY 294002, a phosphatidylinositol (PI)3-kinase inhibitor, to test if the glucose uptake effect was mediated by the insulin signaling pathway. We then used Western blot analysis to re-confirm the result of the insulin signaling inhibition assay. Finally, reporter chimera assay of HuH-7 cells was used to measure the peroxisome proliferator-activated receptor gamma (PPARgamma) activation by BHT.
BHT potentiated insulin-stimulated glucose uptake in 3T3-L1 adipocytes. The effect of BHT-stimulated glucose uptake was neither inhibited by ALLN nor by LY 294002. The protein expression of PI3 kinase pathway did not change after BHT stimulation. PPARgamma activation was elevated by 67.7+/-32% (p<0.05) in HuH-7 cells treated with 0.8 microg/ml of BHT.
BHT stimulated glucose uptake in 3T3-L1 adipocytes. This effect was via PPARgamma activation rather than via the insulin signaling pathway.
一种传统降糖中药复方的分子机制
探讨由知母、石膏、甘草和粳米组成的传统中药复方白虎汤(BHT)的葡萄糖摄取作用及其作用机制。
用溶媒、胰岛素或胰岛素加不同浓度的BHT处理分化的3T3-L1脂肪细胞。进行2-脱氧-[(3)H]葡萄糖摄取试验以测量葡萄糖摄取量。为探究BHT葡萄糖摄取的机制,我们使用了两种胰岛素信号转导抑制剂,N-乙酰亮氨酰亮氨酰正亮氨酸(ALLN),一种钙蛋白酶抑制剂,以及LY 294002,一种磷脂酰肌醇(PI)3-激酶抑制剂,以测试葡萄糖摄取作用是否由胰岛素信号通路介导。然后我们使用蛋白质印迹分析来再次确认胰岛素信号抑制试验的结果。最后,使用HuH-7细胞的报告嵌合体试验来测量BHT对过氧化物酶体增殖物激活受体γ(PPARγ)的激活作用。
BHT增强了3T3-L1脂肪细胞中胰岛素刺激的葡萄糖摄取。ALLN和LY 294002均未抑制BHT刺激的葡萄糖摄取作用。BHT刺激后PI3激酶途径的蛋白表达未发生变化。在用0.8μg/ml BHT处理的HuH-7细胞中,PPARγ激活升高了67.7±32%(p<0.05)。
BHT刺激3T3-L1脂肪细胞摄取葡萄糖。这种作用是通过激活PPARγ而不是通过胰岛素信号通路实现的。