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[Objective] To observe the protective effects of APS-A1 on blood vessel endothelium function induced by isofenphos-methyl. [Method]The ex vivo aorta pectoralis vascular ring (EVAPVR) of rats and cultured human umbilical vein endothelial cells (HUVEC) were exposed to medium contained isofenphos-methyl oxon (7μmol/L), APS-A1 for difference concentration were used to inhibit the damage effect. The endothelial-dependent relaxation reaction (EDRR), endothelial cell monolayer permeability (ECMP), and biochemical index were measured. [Result] APS-A1 dose dependently (0.1, 1, 10 mg/ml) reduced the inhibition of ACh-induced EDRR and the increased ECMP induced by isofenphos-methyl, simultaneously APS-A1(10mg/ml) also protected the SOD activity, inhibited the increase of the MDA content and reduction of NO content induced by isofenphos-methyl in medium of cultured HUVEC. [Conclusion] APS-A1 can protect the blood vessel endothelium function from been impaired by isofenphos-methyl, and the potential mechanism is possibly concerned with the antioxidation of APS-A1.
[Objective] To observe the protective effects of APS-A1 on blood vessel endothelium function induced by isofenphos-methyl. [Method] The ex vivo aorta pectoralis vascular ring (EVAPVR) of rats and cultured human umbilical vein endothelial cells (HUVEC) were exposed The endothelial-dependent relaxation reaction (EDRR), endothelial cell monolayer permeability (ECMP), and biochemical index were measured to inhibit the damage effect. APS-A1 (10 mg / ml) also protected the SODs (APS-A1 dose dependently (0.1, 1, 10 mg / ml) reduced the inhibition of ACh-induced EDRR and the increased ECMP induced by isofenphos- activity, inhibited the increase of the MDA content and reduction of NO content induced by isofenphos-methyl in medium of cultured HUVEC. [Conclusion] APS-A1 can protect the blood vessel endothelium function from been impaired by isofenphos-methyl, and the potenti al mechanism is possibly concerned with the antioxidation of APS-A1.