白介素6拮抗N甲基D天门冬氨酸诱导的神经元凋亡

【摘要】  目的：在抗凋亡成分Bcl-2、促凋亡成分Bax和凋亡关键酶半胱氨酸蛋白酶-3（cysteinyl asparate-specific proteinase-3，caspase-3）的基因水平，探讨IL-6保护神经元防止N-甲基-D-天门冬氨酸（NMDA）诱导的神经元凋亡。方法：取出生后8 d幼鼠的小脑进行颗粒神经元体外培养。在培养液中加入IL-6（40 ng/ml），孵育 8 d后，用NMDA（100 μmol/L）刺激小脑颗粒神经元30 min，诱导神经元凋亡。用Real-time PCR法检测神经元内Bcl-2、Bax和caspase-3的mRNA表达水平。结果：未用IL-6预处理的神经元，在用NMDA刺激后，其表达Bcl-2 mRNA显著减少，表达Bax mRNA及caspase-3 mRNA明显增加。IL-6本身没有明显影响上述基因的表达。神经元用IL-6预孵育后，再用NMDA刺激，神经元内Bcl-2、Bax和caspase-3的mRNA表达水平与未用IL-6预处理的神经元比较，表现为Bcl-2上调、Bax和caspase-3下调的变化，这些变化均有显著意义。结论：NMDA可诱导神经元的凋亡，IL-6对NMDA诱导的神经元凋亡具有明显的抑制作用。

【关键词】  神经元凋亡；白介素-6；N-甲基-D-天门冬氨酸；Bcl-2；Bax；半胱氨酸蛋白酶-3；大鼠

Interleukin-6 prevents NMDA-induced apoptosis of the cultured cerebellar granule neurons

    LIU Zhan， HUANG Huiwei， HUANG Yan，et al      （Department of Physiology， School of Medicine， Nantong University， Nantong 226001）

    [Abstract]   Objective: We explored that IL-6 protected neurons against NMDA-induced apoptosis at the gene levels of anti-apoptotic Bcl-2， pro-apoptotic Bax and apoptotic enzyme cysteinyl asparate-specific proteinase-3 （caspase-3）. Methods: The cerebellar granule neurons from postnatal 8-day infant rats were chronically exposed to IL-6 （40 ng/ml）， NMDA （100 μmol/L） was then added to the cultures and stimulated the neurons for 30 min to induce the neuronal apoptosis. Real-time PCR was employed to detect the expression of genes related to neuronal apoptosis， including Bcl-2， Bax and caspase-3. Results: NMDA stimulation of the cultured cerebellar granule neurons without IL-6 pretreatment led to a notable reduction of Bcl-2 mRNA expression， as well as a remarkable enhancement of Bax and caspase-3 mRNA expression. The NMDA stimulation of the neurons that had been pretreated with IL-6 caused a remarkable increase in Bcl-2 mRNA expression， as well as a marked decrease in Bax and caspase-3 mRNA ex

[1] [2] [3] [4] [5] [6] 下一页