[Objective] The study aimed to explore the protective effects of LBP-Ⅳ on blood vessel endothelium function induced by paraoxon（PARA） and the potential mechanisms. [Method] The ex vivo aorta pectoralis vascular ring （EVAPVR） of rats and cultured human umbilical vein endothelial cells （HUVEC） were exposed to medium contained paraoxon （3.63 μmol/L）, LBP-Ⅳ for different concentration were used to inhibit the damage effect. The endothelial-dependent relaxation reaction （EDRR）, endothelial cell monolayer permeability（ECMP）, biochemical index were measured.[Result] LBP-Ⅳ dose dependently （0.1, 1, 10 mg/ml） reduced the inhibition of ACh-induced EDRR and the increased ECMP induced by PARA, simultaneously LBP-Ⅳ（10 mg/ml） also protected the SOD activity, inhibited the increase of the MDA content and reduction of NO content induced by PARA in medium of cultured HUVEC. [Conclusion] LBP-Ⅳ could protect the blood vessel endothelium function from being impaired by PARA, and the potential mechanism was possibly concerned with the antioxidation of LBP-Ⅳ.
[ Objective] The paper was to explore the effect of astragalin on paraoxon-indueed vascular endothelium dysfunction and analyze the potential mecha- nism. [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 inhib- it the damage effect. Rat thoracic aorta rings were suspended in organ chambers to assess vas orelaxation activity in vitro by acetyleholine （ACh）-induced endotheli- um dependent relaxation reaction （EDRR） and sodium nitroprusside （SNP）-induced endothdium-independent relaxation reaction. [Result]The exposure to parao- xon （3.63 μmol/L） resulted in an inhibition of the EDRR, markedly reduced the level of nitric oxide （NO）, the activity of paraoxonasel （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 PONI.
