Abstract
The aim of this study was to investigate the effect of 2,3,4’,5-tetrahydroxystilbene 2-O-β-D-glucoside (TSG) on vascular endothelial dysfunction in the type 2 diabetes rats, and the possible mechanisms. Sprague-Dawley rats were treated by high-fat diet and intraperitoneal injection of streptozotocin (40 mg/kg) to induce type 2 diabetes. TSG (60 or 120 mg/kg per day) was administered by oral gavage for 6 weeks. The vascular endothelial dysfunction was assessed using isolated aortic ring preparation. Fasting serum insulin (FINS), fasting blood glucose (FBG), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α) and free fatty acids (FFA) in serum were measured. The homeostasis model assessment-insulin resistance (HOMA-IR) was also calculated. The mRNA and protein expression of endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) in the aorta were tested by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western Blot. The results showed that TSG significantly decreased the levels of FBG, HOMA-IR, MDA, TNF-α and FFA and significantly increased the level of SOD. TSG also improved acetylcholine-induced endothelium-dependent relaxation. The expression of eNOS was significantly increased, whereas the expression of ET-1 was significantly decreased in aortas of diabetic rats with TSG treatment. These results demonstrate that TSG prevents vascular endothelial dysfunction in type 2 diabetes rats, and the mechanism may be related to its ability of anti-oxidation, anti-inflammation, improving insulin resistance, up-regulation of eNOS and down-regulation of ET-1. Key words: 2,3,4’,5-Tetrahydroxystilbene2-O-β-D-glucoside, type 2 diabetes, endothelial dysfunction, endothelial nitric oxide synthase, endothelin-1.
Highlights
Type 2 diabetes is characterized by impaired endothelium-dependent relaxation (EDR), which contributes to the high prevalence of vascular disease in such patients
These results demonstrate that tetrahydroxystilbene 2-O-β-D-glucoside (TSG) prevents vascular endothelial dysfunction in type 2 diabetes rats, and the mechanism may be related to its ability of anti-oxidation, anti-inflammation, improving insulin resistance, up-regulation of endothelial nitric oxide synthase (eNOS) and down-regulation of ET-1
fasting blood glucose (FBG), fasting serum insulin (FINS) and homeostasis model assessment-insulin resistance (HOMA-insulin resistance (IR)) were significantly decreased by treatment with TSG (60 or 120 mg/kg/day) compared with the diabetes group (P
Summary
Type 2 diabetes is characterized by impaired endothelium-dependent relaxation (EDR), which contributes to the high prevalence of vascular disease in such patients. EDR injury may be intrinsic to the insulin resistance (IR) that commonly precedes type 2 diabetes (Tooke and Hannemann et al, 2000). Insulin plays an important physiological role in keeping the vascular homeostasis under healthy conditions. The balance between nitric oxide (NO)-dependent vasodilator actions and ET-1-dependent vasoconstrictor actions of insulin is regulated by PI3K- and MAPK-dependent signaling in vascular endothelium, respectively (Yang and Li, 2008; Gogg et al, 2009). The balance is broken and the endothelial dysfunction emerges. The protection of endothelial function has become the key of treatment type 2 diabetes and the vascular complication of the diabetes
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