Effect of combination of ganoderma lucidum polysaccharide and metformin on aortic lesions and expression of VEGF in type 2 diabetic rats
10.3969/j.issn.1001-1978.2014.08.009
- VernacularTitle:灵芝多糖联合二甲双胍预防糖尿病大鼠主动脉病变及对VEGF表达的影响
- Author:
Jin QIAO
;
Zhihua DOU
;
Feng WU
;
Guoliang MENG
;
Hui CHEN
;
Huihua ZHEN
- Publication Type:Journal Article
- Keywords:
ganoderma lucidum polyccharide;
met-formin;
diabetes mellitus rats;
thoracic aorta;
oxidative stress;
VEGF
- From:
Chinese Pharmacological Bulletin
2014;(8):1079-1084
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects and mecha of ganoderma lucidum polysaccharides and metformin on pathological changes of thoracic aorta in diabetic ratsandthemechanisms.Methods SDratswerefed with high fat diet for 4 weeks and injected with strepto-zotocin ( 30 mg · kg-1 ) to replicate type 2 diabetic model. The diabetic rats were randomly into diabetes group, ganoderma lucidum polysaccharides group ( 600 mg·kg-1 ) ,metformin group(600 mg·kg-1 ) ,combi-nation group ( ganoderma lucidum polysaccharides 300 mg· kg-1 + metformin 300 mg · kg-1 ) and normal control group. After 12 weeksˊ treatment, the levels of fasting serum glucose, the activity of catalase(CAT), glutathione peroxidase ( GSH-Px ) , total cholesterol (TC)and triglyceride(TG) in serum were detected. Pathological changes of thoracic aorta were observed by HE staining. Immunohistochemy and Western blot were used to detect thoracic aorta VEGF protein expression. Results Combination group could lower fasting serum glucose and blood fat significantly, meanwhile the ac-tivity of CAT and GSH-Px in serum was improved. The expression of VEGF in thoracic aorta was repressed. The result of HE staining suggested that the lipid de-posits in aortic endothelium in combination group were lessthanthoseinthemodelgroup.Conclusions Ga-noderma lucidum polysaccharides combined with met-formin has an obvious prevention on pathological chan-ges of thoracic aorta in diabetic rats. The possible mechanism may be related to repressing oxidative stress of thoracic aorta, regulating the dyslipidemia, and the down regulation of the expression of VEGF in thoracic aorta.
