Effect of compound Chinese sour taste herbs on advanced glycation end products content and gene expression of their receptors in aorta of rats with type 2 diabetes mellitus.
- Author:
Gui-Xiang YIN
1
;
Yu-Li CAO
;
De-Zeng ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Aorta; metabolism; Diabetes Mellitus, Experimental; drug therapy; metabolism; Diabetes Mellitus, Type 2; drug therapy; metabolism; Drugs, Chinese Herbal; pharmacology; therapeutic use; Glycation End Products, Advanced; metabolism; Male; Phytotherapy; Rats; Rats, Sprague-Dawley; Receptor for Advanced Glycation End Products; Receptors, Immunologic; genetics; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2009;29(8):725-728
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the possible mechanism of compound Chinese sour taste herbs (CS) in preventing and ameliorating diabetic macroangiopathy by analyzing the effects of CS on the deposition of advanced glycation end products (AGEs) and gene expression of receptor for advanced glycation end products (RAGE) in the aorta tissue of rats with type 2 diabetes mellitus (T2DM).
METHODSRat model of T2DM was established by peritoneal injection of streptozotocin (STZ) and high caloric diet feeding. Experimental SD rats were divided into the normal group, the model group, the aminoguanidine (AG) group, and the CS group. At the end of the 8th and 12th week, the fasting blood glucose (FBG) was measured by glucose oxidase method; content of AGEs and collagen in aorta detected by fluorescent method and gene expression of RAGE in aorta determined by Real-time PCR method.
RESULTSFBG, AGEs and collagen contents and RAGE expression in aorta of model rats were all higher than those in the normal control group (P <0.05), while all these indices were lower in the CS group than in the model group (P<0.05).
CONCLUSIONCS could realize the goal for preventing and ameliorating diabetic macroangiopathy by way of suppressing the production of AGEs and down-regulating the gene expression of RAGE in aorta of T2DM rats.
