[Objective] The paper was to explore the effect of astragalin on paraoxon-induced vascular endothelium dysfunction and analyze the potential mechanism. [Method]The isolated rat thoracic aorta rings were exposed to medium contained paraoxon (3.63 μmol/L), and astragalin (10 μmol/L) was used to inhibit the damage effect. Rat thoracic aorta rings were suspended in organ chambers to assess vas orelaxation activity in vitro by acetylcholine (ACh)-induced endothelium dependent relaxation reaction (EDRR) and sodium nitroprusside (SNP)-induced endothelium-independent relaxation reaction. [Result]The exposure to paraoxon (3.63 μmol/L) resulted in an inhibition of the EDRR, markedly reduced the level of nitric oxide (NO), the activity of paraoxonase1 (PON1) and superoxide dismutase (SOD), and significantly increased the level of malondialdehyde (MDA) in isolated rat thoracic aorta. However, the presence of astragalin (10 μmol/L) markedly attenuated the vascular endothelium dysfunction induced by paraoxon via increasing level of NO, activity of PON1 and SOD, as well as reducing level of MDA. In addition, treatment of astragalin (10 μmol/L) showed a similar effect to hydrogen peroxide (1.0 μmol/L), a kind of antioxidant, on paraoxon-induced vascular endothelium dysfunction. [Conclusion]Astragalin could protect the vascular endothelium against the paraoxon-induced dysfunction in isolated rat thoracic aorta, and the beneficial effects of astragalin might be concerned with the antioxidation of astragalin due to inhibiting the decreased activity of PON1.
