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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 investigate the molecular mechanism of endotoxin-induced brain injury by observing the contents of L PO, SOD activity and κBα m RNA expression in brain cortex of rats with endotoxin shock and the effect of panaxadiol saponins (PDS) on it. Methods: Wistar rats were randomly divided into control group, endotoxin shock (L PS) group, dexamethasone (L PS+Dex) group and panaxadiol saponin (L PS+PDS) group. After rats were intravenously injected with endotoxin (4mg·kg-1) for 4 h, the contents of L PO, SOD, and the expression of κBα m RNA in brain tissue were measured. Results: The L PO in L PS+Dex group and L PS+PDS group was significantly lower than that in L PS group (P< 0.05), and the SOD activity was significantly higher than that in L PS group (P< 0.05). The expression of κBαm RNA in L PS+Dex group and L PS+PDS group was higher than that in L PS group (P<0.05). Conclusion: PDS can up-regulate the expression of κBα in brain tissue, reduce the tissue peroxidation induced by endotoxin, and protect the central nervous system (P<0.05).