期刊文献+

生脉注射液对急性百草枯中毒大鼠肝损伤NO和iNOS的影响 被引量:2

Effects of Pulse-activating Injection on NO and iNOS in Rats with Acute Hepatic Injury Induced by Paraquat
下载PDF
导出
摘要 目的:观察百草枯(PQ)急性中毒大鼠所致肝损伤时一氧化氮(NO)和诱导型一氧化氮合酶(iNOS)的变化,探讨生脉注射液对急性百草枯中毒所致肝损伤的保护作用。方法:将50只SD大鼠随机分成5组,空白组、阴性对照组、阳性对照组、生脉低剂量组和生脉高剂量组。观察大体标本,组织病理,测定血清中ALT、AST、MDA、SOD和GSH-Px。同时测定肺组织NO含量和iNOS活性。结果:与阴性对照组相比,生脉低剂量组肝组织病理显示肝出血明显减轻。ALT、AST、MDA、SOD和GSH-Px变化均有统计学意义(P<0.05,P<0.01),NO和iNOS也降低(P<0.01)。结论:NO及iNOS在百草枯所致大鼠肝损伤中起一定作用,生脉注射液能降低NO及iNOS水平,减轻百草枯中毒大鼠肝组织损伤。 Objective: The variance of NO and iNOS on Paraquat induced rat acute hepatic injury was investigated, and the protection of pulse-activating injection on rat acute hepatic injury was approached. Methods: 50 Sprague- Dawley (SD) rats were randomly divided into five experimental groups: blank group, negative control group, positive control group, pulse-activating injection low-dose group(LDG), pulseactivating injection high-dose group(HDG). Microscopical histopathologieal examinations were performed. In the mean time, the level of ALT, AST, MDA, SOD and GSH-Px in plasma were detected, and the activities of liver tissue homogenate NO and iNOS were measured. Results: Compared with that in negativecontrol group,hemorrhage of liver of pulse-activating injection low-dose group were mitigated. ALT、 AST、 MDA、 SOD and GSH-Px in plasma have statistical significance (P〈0.05, P〈0.01 ) ; and biological indexes of hepatic injury and the contents of NO and iNOS were significantly decreased (P〈0.05, P〈0.01 ). Conclusions: NO and iNOS could play an role in hepatic injury of poisoned rats, pulse-activating injection could ameliorate the hepatic injury and decrease the concentrations of NO and iNOS.
出处 《辽宁中医药大学学报》 CAS 2009年第12期192-194,共3页 Journal of Liaoning University of Traditional Chinese Medicine
基金 河北省中医药管理局科研基金资助项目(2008070) 河北省卫生厅科研基金资助项目(08370) 河北大学医学部科学研究基金资助项目(2007Q06)
关键词 生脉注射液 百草枯 肝损伤 一氧化氮 一氧化氮合酶 pulse-activating injection paraquat hepatic injury Nitric oxide lnducible nitric oxide synthase
  • 相关文献

参考文献11

二级参考文献40

共引文献124

同被引文献21

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部