阿魏酸钠对脂多糖引起的大鼠海马损伤的保护作用的信号传导机制

发布时间：2018-05-26 11:26

本文选题：阿魏酸钠 + 阿尔茨海默症　；参考：《中国老年学杂志》2014年01期

【摘要】：目的研究阿魏酸钠(SF)对脂多糖(LPS)所致大鼠海马神经元损伤保护作用的信号传导机制。方法 SD大鼠灌胃给予SF(100,200 mg/kg)3 w后,脑室注射LPS建立损伤模型,对照组灌胃及注射等量生理盐水,Western蛋白印迹观察磷酸化丝裂原激活的蛋白激酶的激酶4(MKK4)、磷酸化c-Jun氨基末端激酶1(JNK1)、磷酸化c-Jun和caspase-3表达,应用荧光免疫组织化学进行p-JNK和OX-42双染,激光共聚焦显微镜观察磷酸化JNK的表达部位。结果与LPS损伤组比较SF(100,200 mg/kg)能对抗LPS引起的海马CA1区磷酸化MKK4、磷酸化JNK1和磷酸化c-Jun及caspase-3表达水平增加(P0.05),激光共聚焦显微镜观察结果显示,磷酸化的JNK主要在小胶质细胞表达。结论 SF通过抑制JNK激酶信号传导通路的活化,对抗LPS引起的海马炎症反应。
[Abstract]:Objective to study the signal transduction mechanism of the protective effect of sodium ferulate (SF) on rat hippocampal neuron injury induced by lipopolysaccharide (LPS). Methods SD rats were injected with SF (100200 mg/kg) and 3 w to establish the injury model by intraventricular injection of LPS, and the control group was injected with the same amount of normal saline, and the protein activated by phosphorylated mitogen was observed by Western blotting. Kinase 4 (MKK4), phosphorylated c-Jun amino terminal kinase 1 (JNK1), phosphorylated c-Jun and Caspase-3 expression, p-JNK and OX-42 double staining with fluorescent immunohistochemistry. The expression of phosphorylated JNK is observed by laser confocal microscopy. The results are compared with LPS damage group and SF (100200 mg/kg) can antagonize the phosphorylation of hippocampal regions caused by LPS. 4, the expression level of phosphorylated JNK1 and phosphorylated c-Jun and caspase-3 increased (P0.05). The results of laser confocal microscopy showed that the phosphorylated JNK was mainly expressed in the microglia. Conclusion SF could antagonism the reaction of hippocampal induced by LPS by inhibiting the activation of JNK kinase signaling pathway.
【作者单位】：辽宁医学院药理学教研室;辽宁医学院机能实验中心;
【基金】：辽宁省教育厅科学研究项目(No.L2012310)
【分类号】：R749.16

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