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Relationship between heat stress suppression of neuroapoptosis and activation of nuclear kappa B in primary cultured rat cerebellar granule cells
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- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 3
- DOI:
- 10.3321/j.issn:0371-0874.2001.03.006
- Key Word:
- 核因子热应激;小脑颗粒神经元;凋亡
Abstract： 实验采用低钾诱导大鼠小脑颗粒神经元凋亡模型,观察核因子kappa B (NF-kappa B)活性与热应激抑制神经元凋亡之间的关系.迁移率改变法(EMSA)检测结果显示:神经元经低钾处理16 h可见NF-kappa B活性明显升高,热应激处理可减弱低钾诱发的NF-kappa B激活,并呈时间依赖性.Hoechst 33258荧光素核染色、DNA琼脂糖凝胶电泳和流式细胞(FCM)检测均发现低钾16 h可诱发神经元凋亡,预先用热处理60或90 min可明显减弱低钾诱发的神经元凋亡.用佛波酯(PMA)激活NF-kappa B,可进一步增强60 min热应激抑制神经元凋亡的作用,而用吡咯烷二硫代氨基甲酸盐(PDTC)选择性阻断NF-kappa B活性后,热应激抑制神经元凋亡的作用明显减弱.上述结果提示,热应激的神经保护作用与减弱NF-kappa B活性无关,而NF-kappa B激活可能参与了热应激抑制神经元凋亡的作用.
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