Key result
TSG improves endothelium-dependent relaxation and preserves nitric oxide bioactivity in atherogenic-diet rats.
Why the study?
The potential of 2,3,4',5-Tetrahydroxystilbene 2-O-beta-D-glucoside (TSG) to prevent atherosclerosis by improving endothelial function in atherogenic-diet rats was investigated.
Extends TSG endothelial data in atherogenic rats; hypothesis-generating and should not change clinical practice.
2,3,4',5-Tetrahydroxystilbene 2- O-beta- D-glucoside (TSG), an active component extracted from Polygonum multiflorum, has been found to have an anti-atherosclerotic effect. The aim of this study was to investigate whether the TSG could prevent the development of atherosclerosis through influencing endothelial function in atherogenic-diet rats and to explore the possible mechanisms. Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, transmission electron microscopy of the aorta, and levels of nitrate/nitrite (NOx) in serum and aorta. Endothelial nitric oxide (NO) synthase (eNOS) and inducible NO synthase (iNOS) mRNA and protein expression were also measured. After 12 weeks treatment, TSG improved acetylcholine-induced endothelium-dependent relaxation, prevented intimal remodeling, inhibited the decreased NOx content in serum and aorta in atherogenic-diet rats. Furthermore, the observed decreased eNOS mRNA and protein expression and increased iNOS mRNA and protein expression in atherogenic-diet rats were attenuated by TSG treatment. These results suggest that TSG could restore vascular endothelial function, which may be related to its ability to prevent changes of eNOS and iNOS expression, leading to preservation of NO bioactivity.
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Zhang et al. (2009) studied Vascular endothelial dysfunction and atherosclerosis. 2,3,4',5-Tetrahydroxystilbene 2-O-beta-D-glucoside (TSG) vs. Untreated atherogenic-diet rats was evaluated on Vascular endothelial dysfunction (acetylcholine-induced endothelium-dependent relaxation and NOx levels). TSG improved acetylcholine-induced endothelium-dependent relaxation, prevented intimal remodeling, and preserved nitric oxide bioactivity in atherogenic-diet rats after 12 weeks of treatment.
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