摘要
目的 :通过观察内毒素休克大鼠脑皮质中 L PO含量、 SOD活力和 κBα m RNA表达及人参二醇组皂苷 (PDS)对其的影响 ,探讨内毒素引起脑组织损伤的分子机制。方法 :Wistar大鼠随机分为对照组、内毒素休克 (L PS)组、地塞米松 (L PS+Dex)组和人参二醇组皂苷 (L PS+PDS)组。大鼠静脉注射内毒素 (4mg· kg- 1 )4 h后测定脑组织中 L PO含量、 SOD活力及 κBα m RNA的表达。结果 :L PS+Dex组和 L PS+PDS组 L PO显著低于 L PS组 (P<0 .0 5 ) ,SOD活力明显高于 L PS组 (P<0 .0 5 )。 L PS+Dex组和 L PS+PDS组 κBαm RNA表达高于 L PS组 (P<0 .0 5 )。结论 :PDS能够上调脑组织中 κBα的表达 ,减轻内毒素引起的组织过氧化反应 ,对中枢神经系统具有保护作用 (P<0 .0 5 )。
Objective To explore the molecular mechanism of brain tissue injury induced by endotoxin through observation of LPO content, SOD activity, and ⅠκBα mRNA expression of cortex in endotoxic shock rats. Methods Wistar rats were randomly divided into lipopolysaccharide(LPS), LPS+dexamethasone(Dex), LPS+panaxadiol(PDS) and control group, respectively. The LPO content, SOD activity, and ⅠκBα mRNA expression were assayed 4 h after intravenous injection of LPS. Results MDA contents in LPS+Dex and LPS+PDS groups were obviously lower than that in LPS group (P<0.05), and the SOD activities were significantly higher than that in LPS group (P<0.05). Compared with the control group, ⅠκBα mRNA expressions in LPS+Dex and LPS+PDS groups were significantly higher than that in LPS group (P<0.05). Conclusion PDS may up-regulate ⅠκBα expression in the brain tissue, release the tissue peroxidation reaction induced by endotoxin and protect the central nervous system.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2005年第1期42-44,共3页
Journal of Jilin University:Medicine Edition
基金
吉林省科技厅自然科学基金资助课题 (2 0 0 30 5 0 1)