Intervention of Ganoderma lucidum polysaccharide combined with metformin on AGEs and CTGF in thoracic aorta of diabetic rats
10.7501/j.issn.0253-2670.2014.20.014
- Author:
Jin QIAO
1
Author Information
1. Department of Pharmacy, The Third People's Hospital of Nantong
- Publication Type:Journal Article
- Keywords:
AGEs;
CTGF;
Diabetes mellitus;
Ganoderma Lucidum polyccharides;
Metformin;
Oxidative stress;
Thoracic aorta
- From:
Chinese Traditional and Herbal Drugs
2014;45(20):2939-2945
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To study the effects of Ganoderma lucidum polysaccharides (GLPs) and metformin (Met) on the expression of advanced glycosylation end products (AGEs) and connective tissue growth factor (CTGF) in thoracic aorta of diabetic rats. Methods: SD rats were fed with high fat diet for 4 weeks, and injected with streptozotocin (STZ, 30 mg/kg) to establish type 2 diabetic model. The diabetic rats were randomly divided into diabetes group, GLPs group (600 mg/kg), Met group (600 mg/kg), combination group (GLPs 300 mg/kg + Met 300 mg/kg), and normal control group. After 12 weeks' treatment, the levels of fasting serum glucose, insulin in plasma, AGEs in serum, the activity of catalase (CAT) and glutathione peroxidase (GSH-Px) were detected. The pathological changes of thoracic aorta were examined by electron microscope. Immunohistochemical and Western blotting methods were used to detect AGEs and CTGF protein expression in thoracic aorta. Results: Combination group could lower the fasting blood glucose significantly, raise the insulin level in plasma, improve the activity of CAT and GSH-Px in myocardium, decrease the concentration of AGEs in serum, reduce the expression of AGEs and CTGF in thoracic aorta, and relieve the pathological change process of thoracic aorta. Conclusion: GLPs combined with Met shows the protective effect on the thoracic aorta in diabetic rats. The possible mechanism may be related to inhibit the oxidative stress of thoracic aorta, lower AGEs level in serum, and do some down regulation of AGEs and CTGF in thoracic aorta.
