摘要
目的 观察葛根素 (Puerarin ,Pue)对糖尿病 (DM)大鼠主动脉糖基化终产物 (AGEs)的形成及其受体 (RAGEmRNA)表达的影响。方法 以STZ诱导DM大鼠模型 ,并将DM大鼠随机分为DM对照组 (DM)、不同剂量葛根素治疗组 (0 5、0 2 5、0 1 2 5g·kg-1 ,ig )和氨基胍治疗组 (0 1g·kg-1 ,ig) ,另设一正常对照组 ,给药 1 2wk后 ,分别以葡萄糖氧化酶法测定血糖 ,NBT法测定血清果糖胺的含量 ,采用荧光法、RT PCR方法分别对主动脉AGEs的沉积及RAGEmRNA的表达进行检测。结果 Pue治疗后DM大鼠血糖、血清果糖胺含量明显降低 ,主动脉AGEs的形成量也明显低于DM模型组 (P <0 0 1 ) ,其治疗作用与氨基胍 (AG)相当 ;RAGE主要在内皮细胞表达 ,其表达量与AGEs的沉积量呈明显正相关 ,而葛根素也可明显下调RAGEmRNA在DM大鼠主动脉中的表达 (P<0 0 1 )。结论 葛根素可通过有效降低糖尿病大鼠血糖、血清果糖胺的含量 ,减少主动脉AGEs的沉积 ,下调主动脉中RAGEmRNA的表达 。
AIM To investigate the effect of puerarin on the formation of advanced glycation end products (AGEs) and RAGE(receptor for advanced glycation end products)mRNA expression in the arota of diabetic rats induced by streptozotocin (STZ). METHODS Rats were injected streptozotocin into intraperitonel with a dose of 60 mg·kg -1 . Four days later, blood glucose was measured using glucose oxygen kit. The rats with over 16 7 mmol·L -1 blood glucose were considered as diabetic ones, and then divided randomly into five groups: diabetic mellitus(DM), aminoguanidine(AG 0 1 g·kg -1 , ig), pue1(0 5 g·kg -1 , ig), pue2(0 25 g·kg -1 , ig) and pue3(0 125 g·kg -1 , ig). In order to set up a chronic model, we observed 12 weeks according to our past experiments. The fasting blood glucose(FBG) was and the contents of serum fructosamine (FMN) were measured using the test kit. The quantity of AGEs accumulation, the expression of RAGE in the arota was detected using fluorescence method and reverse transcription polymerase chain reaction(RT PCR). RESULTS The contents of FBG and FMN, the accumulation of AGEs in the aorta of rats treated with puerarin were lower than that of diabetic model rats( P <0 01) and were equivalent to that of the AG treatment rats. The expression of RAGE occurred mainly in endothelial cells. The RAGE expression positively correlated with the quantity of AGEs ( P <0 01). CONCLUSION The results suggest that puerarin may decrease the contents of FBG and FMN, reduce AGEs accumulation and also the expression of RAGE in the arota of diabetic rats. It is beneficial to preventing and curing diabetic vascular defects by inhibiting the arotic nonenzymatic glycation in diabetic rats.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2004年第4期393-397,共5页
Chinese Pharmacological Bulletin
基金
江苏省中医药管理局科研基金资助项目
NoH 0 2 8