首页> 外文期刊>Life sciences >PENTAMIDINE DOES NOT INTERFERE WITH NITRITE FORMATION IN ACTIVATED RAW 264.7 MACROPHAGES BUT INHIBITS CONSTITUTIVE BRAIN NITRIC OXIDE SYNTHASE
【24h】

PENTAMIDINE DOES NOT INTERFERE WITH NITRITE FORMATION IN ACTIVATED RAW 264.7 MACROPHAGES BUT INHIBITS CONSTITUTIVE BRAIN NITRIC OXIDE SYNTHASE

机译:戊胺定不干扰活化的RAW 264.7巨噬细胞中亚硝酸盐的形成,但抑制了组成型脑一氧化氮合酶

获取原文
获取原文并翻译 | 示例
           

摘要

Pentamidine effects on the interferon-gamma- or interferon-gamma plus bacterial lipopolysaccharide-induction of nitric oxide synthase in the macrophage cell line RAW 264.7, determined by measuring nitrite release into culture supernatants, were investigated. At concentrations above 10 mu M, pentamidine caused visible toxic effects including cell lysis which also was assessed by measuring lactic dehydrogenase release. A progressive inhibitory effect of pentamidine could not be clearly dissociated from these toxic and lyric effects which were extensive at 100 mu M. At 1 mu M pentamidine, the dose response dependence of nitrite formation on interferon-gamma was not affected. Tumor necrosis factor-alpha caused some enhancement of interferon-gamma-induced nitrite release only at high doses of 100 and 10,000 unit/ml. Pentamidine had no effect on isolated inducible nitric oxide synthase from RAW 264.7 cells but inhibited the constitutive enzyme from pork cerebellum non-competitively. The lack of any stimulatory effect of pentamidine on nitrite production in RAW 264.7 cells suggests that NOS induction and NO production by macrophages is not the mechanism of the antimicrobial effects of this drug. [References: 19]
机译:研究了喷他ite对巨噬细胞系RAW 264.7中一氧化氮合酶的干扰素-γ或干扰素γ加上细菌脂多糖诱导的影响,方法是测量亚硝酸盐向培养上清液的释放。在高于10μM的浓度下,喷他idine引起可见的毒性作用,包括细胞裂解,这也可以通过测量乳酸脱氢酶的释放来评估。喷他idine的渐进抑制作用不能与这些毒性和抒情作用(在100μM时广泛存在)明显分离。在1μM喷他idine中,亚硝酸盐形成对干扰素-γ的剂量反应依赖性没有受到影响。肿瘤坏死因子-α仅在100和10,000单位/毫升的高剂量下才引起干扰素-γ诱导的亚硝酸盐释放的增强。喷他idine对从RAW 264.7细胞分离的诱导型一氧化氮合酶没有影响,但非竞争性地抑制了来自猪小脑的组成型酶。喷他idine对RAW 264.7细胞中亚硝酸盐的产生没有任何刺激作用,这表明巨噬细胞对NOS的诱导和NO的产生不是该药物抗菌作用的机制。 [参考:19]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号