在大鼠缺镁期间，中性内肽酶的抑制会增强中性粒细胞的激活。
Inhibition of neutral endopeptidase potentiates neutrophil activation during Mg-deficiency in the rat.
作者信息
Mak I T, Kramer J H, Chmielinska J J, Khalid M H, Landgraf K M, Weglicki W B
机构信息
Department of Biochemistry & Molecular Biology, Division of Experimental Medicine, George Washington University Medical Center, 2300 Eye St. NW, Ross Hall, Rm 443, Washington, DC 20037, USA.
出版信息
Inflamm Res. 2008 Jul;57(7):300-5. doi: 10.1007/s00011-007-7186-z.
Neutral endopeptidase (NEP), which degrades substance P (SP), may regulate neutrophil activation during Mg-deficiency (MgD). Male Sprague-Dawley rats (180g) were fed MgD (approximately 50 mg Mg/kg) or Mg-sufficient (MgS, 608 mg Mg/kg) diets for 7 days +/- NEP inhibitor phosphoramidon (PR, 5 mg/kg/day, s.c.). MgD alone induced a 9-fold (vs. MgS, p <0.01) elevation in plasma SP; MgD+PR enhanced it further to 18-fold (p <0.001). Neutrophils from MgD+PR rats displayed a 3.9-fold higher (p <0.01) basal .O(2-) generation, but those from MgD or PR alone were not activated. Plasma PGE2-metabolite levels rose 2.67- (p <0.01) and 1.56- (p <0.05) fold, respectively, in MgD+PR and MgD groups; the corresponding red blood cell glutathione levels were decreased 21% (p <0.025) and 7% (NS). MgD+PR significantly reduced neutrophil NEP activity by 48% (p <0.02); PR or MgD alone only reduced this activity 26% and 15%, respectively. We conclude that NEP inhibition potentiates SP-mediated neutrophil .O(2-) production and may promote other inflammatory activities during MgD.
中性内肽酶（NEP）可降解P物质（SP），在镁缺乏（MgD）期间可能调节中性粒细胞的激活。将雄性Sprague-Dawley大鼠（180g）喂食MgD（约50mg镁/千克）或镁充足（MgS，608mg镁/千克）饮食7天，±NEP抑制剂磷酰胺（PR，5mg/千克/天，皮下注射）。单独的MgD可使血浆SP升高9倍（相对于MgS，p<0.01）；MgD+PR使其进一步升高至18倍（p<0.001）。来自MgD+PR大鼠的中性粒细胞基础超氧阴离子（.O(2-)）生成量高3.9倍（p<0.01），但来自单独MgD或PR组的中性粒细胞未被激活。MgD+PR组和MgD组的血浆前列腺素E2代谢物水平分别升高2.67倍（p<0.01）和1.56倍（p<0.05）；相应的红细胞谷胱甘肽水平分别降低21%（p<0.025）和7%（无统计学意义）。MgD+PR使中性粒细胞NEP活性显著降低48%（p<0.02）；单独的PR或MgD仅分别降低该活性26%和15%。我们得出结论，NEP抑制增强了SP介导的中性粒细胞超氧阴离子生成，并可能在MgD期间促进其他炎症活动。
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