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作 者:田维[1] 蔡晓月[1] 王子旭[1] 柳威[1] 王威[1]
出 处:《药物生物技术》2011年第2期138-144,共7页Pharmaceutical Biotechnology
摘 要:探讨复方中药改善血糖和血脂的机制。选用雄性KK-Ay小鼠32只,随机分为空白对照组、中药高剂量组0.7 mg/kg、中药中剂量组0.35 mg/kg、中药低剂量组0.175 mg/kg,灌胃6周。测定血糖和TG、TC等生化指标,并进行葡萄糖耐受性试验。取小鼠肝脏及骨骼肌进行RT-PCR。结果:利湿方剂组TG、TC,LDL、葡萄糖耐量曲线下面积均比对照组显著降低,HDL升高(P<0.05,P<0.01)。基因表达显示中药组AMPK、AdipoR和PPAR-α上调,TNF-α下调,但在肝脏和骨骼肌中的表达有所差异。结论:复方中药能有效降低KKAy小鼠TG、TC,LDL,升高HDL,可能通过上调PPAR-α机制。血糖降低可能与脂联素通过活化AMP激活的蛋白激酶,引起下游信号传导的改变,从而改善胰岛素抵抗。To explore the mechanism of Turbidity-dampness formula to improve blood glucose and lipids.Male KK-Ay mice(n=32) were randomly divided into control group,0.7mg/kg high dose group,0.35mg/kg group,and 0.175mg/kg low dose group,orally for 6 weeks.Blood glucose and TG,TC concentrations were assayed,then the glucose and insulin tolerance test were performeds.Total RNA was extracted from the liver and skeletal muscle tissues and gene expression was determined by RT-PCR.Results showed that in the turbidity-dampness formula groups,TG,TC,LDL,curve area of glucose tolerance was significantly lower than that of the control group,HDL increased(P0.05,P0.01).Gene expression showed that AMPK,AdipoR and PPAR-α increased,TNF-α decreased in the turbidity-dampness formula groups,but the expression was significant different between liver and skeletal muscle.Turbidity-dampness formula can reduce KKAy mice TG,TC,LDL and increase HDL,which may be due to an increase in the PPAR-α.The decreased blood glucose may be related to adiponectin through the activation of AMP-activated protein kinase,causing changes in the downstream signal transduction;it also may be attributed to tumor necrosis factor TNF-α level of improving insulin resistance.
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