氧化应激在D5多巴胺受体基因敲除小鼠血压升高中的作用研究
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Q554


The Mechanism of Dopamine D5 Receptor Regulation Hypertension via NADPH Oxidase
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    摘要:

    目的探讨还原型辅酶Ⅱ(NADPH)氧化酶在D5受体基因敲除(D5-/-)小鼠血压升高发生机理中的作用.方法利用第六代D5-/-小鼠和其对照(D5+/+)小鼠,检测其肾脏NADPH氧化酶的活性和表达;利用D5受体基因转染的HEK-293细胞作为研究对象,刺激D5受体,研究D5受体对超氧阴离子(O2^-)和过氧化氢(H2O2)的影响.结果 D5-/-小鼠的血压、肾脏NADPH氧化酶的活性和p47^phox蛋白的表达均明显高于D5+/+小鼠.多巴胺D5受体激动剂Fenoldopam可降低D5转染HEK-293细胞的O2^-和H2O2的产量.结论氧化应激和NADPH氧化酶活性增强参与了D5-/-小鼠血压升高的发生过程,多巴胺D5受体具有抗氧化应激的功能.

    Abstract:

    Objective To investigate the mechanism(s) of dopamine D_5 receptor regulation to hypertension involved in the antioxidant actions.Methods We investigated blood pressures in D_5 receptor deficient(D_5-/-) and wild type(D_5 / ) mice,and NADPH oxidase protein expression(p47~(phox)) and activity in kidney of those mice.We also checked super oxide and hydrogen peroxide production by using HEK-293 cells heterologously expressing human D_5 receptor.Result The systolic,diastolic and mean arterial blood pressures,and NADPH oxidase activity and p47~(phox) expression were higher in D_5-/-than D_5 / mice.In HEK-293 cells heterologously expressing human D_5 receptor,its agonist,fenoldopam,decreased super oxide and hydrogen peroxide production.Conclusion\ The ability of D_5 receptor stimulation to inhibit NADPH oxidase activity so as to decrease ROS production may explain,in part,the antihypertensive action of D_5 receptor activation.

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杨志伟,曾春雨,秦川.氧化应激在D5多巴胺受体基因敲除小鼠血压升高中的作用研究[J].中国比较医学杂志,2006,(3):129~134,F0002.

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  • 收稿日期:2006-02-23
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