人参二醇组皂苷(PDS)抑制NOS和p38减轻LPS休克脑损伤  

Protective effect of panaxadiols against brain injury induced by LPS through inhibiting NOS activity and p38 expression

作　　者：孙际童[1] 李洪岩[2] 苏静[2] 孔晓霞[2] 禹彬[2] 孙连坤[2] 康劲松[2] 

机构地区：[1]吉林大学公共卫生学院信息系统与信息管理系,吉林长春130021 [2]吉林大学基础医学院病理生理学教研室,吉林长春130021

出　　处：《中国病理生理杂志》2008年第1期44-46,共3页Chinese Journal of Pathophysiology

基　　金：吉林省中医药管理局中医药科学技术研究基金资助项目(No.2004-080)

摘　　要：目的:探讨人参二醇组皂苷(PDS)对LPS诱导休克脑的保护机制。方法:将大鼠随机分为对照组、LPS组、LPS+地塞米松组及LPS+人参二醇皂苷组。大鼠静脉注射LPS(4mg/kg)4h后,测定大脑皮质中NOS的活性、NO的含量及磷酸化p38蛋白的表达。结果:LPS组脑皮质中NOS活性、NO含量及p38的蛋白表达水平明显高于control组,而LPS+Dex组和LPS+PDS组脑皮质中NOS活性、NO含量及p38的蛋白表达水平明显低于LPS组。结论:PDS减轻LPS脑损伤与降低脑皮质中NOS活性、NO含量有关,可能涉及p38MAPKs信号转导通路。AIM： To explore the protective effect of panaxadiols （PDS） on brain injury induced by endotoxin and its mechanism. METHODS： Rats were divided into control, LPS, LPS ＋ dexamethasone （DEX） and LPS ＋ PDS group, respectively. NOS activity, NO content and phosphorylated p38 expression in brain cortex were assayed 4 h after intravenous injection of LPS. RESULTS： NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS group were obviously higher than those in LPS group. NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS ＋ DEX and LPS ＋ PDS groups were obviously lower than those in LPS group. CONCLUSION ： The protective effects of PDS against brain injury induced endotoxin may be related to decreasing NOS activity, NO content in the brain tissue, and this process is involved in p38MAPKs signal transduction.

关 键 词：脂多糖类 人参 地塞米松 P38MAP激酶 一氧化氮合酶 一氧化氮 

分 类 号：R363[医药卫生—病理学]