【摘要】 目的:观察氧自由基（OFR）对体外培养的人脐静脉内皮细胞（HUVECs）产生内源性一氧化氮合酶抑制剂——非对称型二甲基精氨酸（ADMA）的影响及葛根素的干预作用。方法:以黄嘌呤氧化酶作用于次黄嘌呤产生的 OFR 作用于培养的 HUVECs;并加用葛根素进行干预,以高效液相色谱法（HPLC）和经流式细胞仪检测细胞培养液中 ADMA、L-arg 和细胞内游离钙水平,并测定一氧化氮（NO）及内皮素（ET）的含量。结果:OFR 使培养液中 ADMA、ET 含量显著增加,而 NO 水平则降低,并使胞质内[Ca²⁺]i 浓度升高;加用葛根素后,ADMA 明显减少,NO 合成增加,细胞内[Ca²⁺]i 显著降低。结论:OFR 能通过增加 ADMA 使NO 合成减少,葛根素能通过减少 ADMA 而抑制 OFR 导致的内皮细胞功能障碍。更多还原

【Abstract】 Objective:To observe the effect of oxygen free radical （OFR） and Puerarin intervention on production of endogenous nitrogen oxide synthase inhibitor,the asymmetrical dimethylarginine （ADMA） in cultured human umbilical vein endothelial cells （HUVECs）. Methods:HUVECs cultured with OFR （0.01mmol/L,0.1mmol/L） produced by xanthine on hypoxauthine and intervened with Puerarin （0.5mg/ml）.The levels of ADMA and L-Arg in the conditioned medium were measured by HPLC,NO,ET were mea- sured by the test kit respectively.The contents of cytosolic free calcium[Ca²⁺]i were determined by flow cytometry.Results:OFR significantly increased the level of ADMA,ET and content of cytosolic free calcium[Ca²⁺]i,but decreased the concentration of NO in conditioned medium.However,the level of L-Arg was not significantly changed.When added Puerarin,the levels of ADMA and cy- tosolic free calcium[Ca²⁺]i were markedly decreased,NO was increased markedly.Conclusion:OFR can induce the production of ADMA,which may contribute to the metabolism dysfunction of endothelial ceils,the abnormality of this kind of metabolism dysfunc- tion of endothelial cells can be inhibited by Puerarin.更多还原