• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Reactive oxygen and nitrogen species modulate the ex-vivo effects of LPS on platelet adhesion to fibrinogen.
【24h】

Reactive oxygen and nitrogen species modulate the ex-vivo effects of LPS on platelet adhesion to fibrinogen.

机译：活性氧和氮物质可调节LPS对血小板粘附到纤维蛋白原的体外作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

AIMS: Excessive production of nitric oxide (NO) and reactive oxygen species (ROS) in sepsis modulates different cell functions. Since the sepsis severity is associated with the degree of platelet activation, we decided to investigate the role of systemic generation of NO and ROS in modulating the platelet adhesion of lipopolysaccharide (LPS)-treated rats. MAIN METHODS: Platelet adhesion was evaluated using fibrinogen-coated 96-well microtiter plates. Cyclic GMP levels were measured using enzyme immunoassay kit. KEY FINDINGS: Treatment of rats with LPS significantly increased spontaneous platelet adhesion, but reduced the thrombin-activated platelet adhesion when compared with control rats. Chronic treatment of rats with the NO synthase inhibitor L-NAME (20 mg/rat/day, 7 days) prior to LPS injection normalized the increased adhesion in non-activated platelets, but failed to affect the adhesion in thrombin-activated platelets. The cGMP levels were modified neither in non-activated nor in thrombin-activated platelets of LPS-treated rats when compared with control rats. The incubation of non-activated platelets with the O2- scavenger PEG-SOD reversed the stimulatory effect of LPS on spontaneous adhesion, but had no effect in stimulated-platelet adhesion of non-treated or LPS-treated groups. Moreover, pretreatment of rats with the antioxidant N-acetylcysteine (NAC; 150 mg/kg) prevented the increase of non-activated platelet adhesion, and significantly reduced the inhibitory effect of LPS on thrombin-stimulated adhesion. SIGNIFICANCE: Our findings suggest that in LPS-treated rats, NO plays an important modulatory role only in non-stimulated platelet adhesion through cGMP-independent mechanisms, while ROS, directly or by affecting the redox state of the animals, modulates both non-activated and thrombin-activated platelet adhesion.
机译：目的：脓毒症中一氧化氮（NO）和活性氧（ROS）的过量产生可调节不同的细胞功能。由于败血症的严重程度与血小板活化程度有关，我们决定研究全身性产生NO和ROS在调节脂多糖（LPS）处理的大鼠的血小板粘附中的作用。主要方法：使用纤维蛋白原包被的96孔微量滴定板评估血小板粘附性。使用酶免疫测定试剂盒测量循环GMP水平。主要发现：与对照组大鼠相比，LPS处理的大鼠明显增加了自发性血小板粘附，但降低了凝血酶激活的血小板粘附。在LPS注射之前用NO合酶抑制剂L-NAME（20 mg /大鼠/天，7天）对大鼠进行长期治疗，可以使未激活的血小板粘附增加，但不能影响凝血酶激活的血小板的粘附。与对照大鼠相比，LPS处理的大鼠的未激活血小板和凝血酶激活血小板中的cGMP水平均未改变。未活化的血小板与O2-清除剂PEG-SOD的孵育逆转了LPS对自发粘附的刺激作用，但对未处理或LPS处理组的刺激性血小板粘附没有影响。此外，用抗氧化剂N-乙酰半胱氨酸（NAC; 150 mg / kg）预处理大鼠可防止未激活的血小板粘附增加，并显着降低LPS对凝血酶刺激的粘附的抑制作用。意义：我们的发现表明，在LPS处理的大鼠中，NO仅通过cGMP依赖性机制仅在非刺激的血小板粘附中起重要的调节作用，而ROS直接或通过影响动物的氧化还原状态来调节非活化的血小板。和凝血酶激活的血小板粘附。

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