期刊文献+

脂多糖诱导小鼠肝损伤介质水平变化及五灵胶囊的作用

The Change of Mediator Levels in Liver Injured Mice Induced by LPS and Effects of Wuling Capsule
下载PDF
导出
摘要 目的探讨脂多糖(LPS)诱导小鼠肝损伤介质水平变化及五灵胶囊的作用。方法小鼠尾静脉注射(iv)LPS 3.5mg/kg,酶法检测3,6,12和24 h小鼠血清ALT、AST、ALP、TRIG,化学法测定肝组织内MDA、NOS水平,免疫组化检测肝组织内TNF-α,CD14,iNOS,eNOS的阳性表达率。结果与正常组比较,小鼠iv注射LPS后3 h血清ALT,AST水平明显升高并持续至12 h,24 h下降仍显著高于正常组,ALP水平明显持续下降。在12 h MDA含量显著升高,24 h下降但明显高于正常组,而甘油三酯(TG)水平各时间点明显升高,TNF-α,CD14,iNOS,eNOS阳性表达率上调。五灵胶囊能明显降低ALT,AST水平和MDA含量,对ALP和TRIG水平无作用,抑制肝组织内TNF-α,CD14,iNOS,eNOS阳性表达率。结论MDA,TNF-α,CD14,iNOS,eNOS参与了LPS诱导肝损伤,五灵胶囊抑制LPS诱导肝损伤的作用机制与抑制活性递质生成有关。 Objective To explore the change of mediator levels in hepatic injured mice induced by Lipoplysaccharide(LPS) and effects of Wuling capsule.Methods LPS was given to mice by injection with a dose of LPS 3.5mg/kg via the tail vein,3,6,12,24 hours later,the levels of ALT,AST,ALP in serum were detected by enzyme method and the contents of MDA,NOS in hepatic tissue of mice were determined by chemistry,immunohistochemistry method was employed to determine the expression of TNF-α,CD14,iNOS and eNOS in hepatic tissue.Results 3 hours after LPS was given to mice,compared with normal group,the levels of ALT and AST were obviously elevated and persisted for 12 hours,and which were reduced in 24 hours but still high obviously as compared with normal group.The level of ALP were evidently decreased,and the content of MDA was significantly increased at 6 hour and lowered at 24 hours but still higher than normal.The level of triglycerides was increased and the expression of TNF-α,CD14,iNOS,eNOS in liver injury tissue was markedly up-regulated.Conclusion The mediators as MDA,TNF-α,CD14,iNOS,eNOS participated in liver injury induced by LPS,the protective mechanism Wuling capsule liver injury might be related with inhibiting the release of mediators.
出处 《时珍国医国药》 CAS CSCD 北大核心 2009年第10期2590-2592,共3页 Lishizhen Medicine and Materia Medica Research
关键词 肝损伤 一氧化氮合酶 活性介质 脂多糖 Liver injury Nitric oxide synthase Activity mediators Lipoplysaccharid
  • 相关文献

参考文献6

二级参考文献16

共引文献57

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