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诱导型一氧化氮合酶在强啡肽致脊髓损伤中的作用 |
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胡文辉 杨慧芬 强文安 孙秀君 刘 娜 万选才 刘景生 任民峰 李 芳 王国强 肖 剑 廖维宏
摘 要 目的：探讨诱导型一氧化氮合酶(iNOS)在强啡肽致脊髓损伤中的作用。方法：［3H］-左旋精氨酸转化法测定腹侧和背侧脊髓iNOS活性，原位杂交法观测脊髓iNOS mRNA表达及其细胞分布。结果：大鼠蛛网膜下腔注射(InI)强啡肽A1-17(Dyn) 20 nmol引起持久性截瘫和迟发性神经元死亡；在Dyn致瘫后2～3 h iNOS mRNA表达开始增多增强，4 h达高峰，24 h和48 h仍见广泛表达，其分布以胶质细胞和大运动神经元为主；腹侧脊髓iNOS活性在Dyn致瘫后4 h显著升高，并持续至24 h和48 h；提前10 min InI选择性iNOS抑制剂氨基胍1 μmol可显著对抗Dyn 20 nmol引起的持久瘫及伤后4 h腹侧脊髓iNOS活性升高。结论：iNOS持续性高表达与Dyn致脊髓损伤机制有关。
主题词 强啡肽；一氧化氮；脊髓损伤
Increases of inducible nitric oxide synthase activity and mRNA expression in rat spinal cord after dynorphin neurotoxicity
HU Wen-Hui, YANG Hui-Fen, LI Fang, QIANG Wen-An, SUN Xiu-Jun, LIU Na,
WAN Xuan-Cai, LIU Jing-Sheng, REN Min-Feng, WANG Guo-Qiang, XIAO Jian, LIAO Wei-Hong
Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing(100005)
Abstract AIM:To explore the role of inducible nitric oxide synthase (iNOS) in dynorphin-induced spinal cord injury. METHODS:The iNOS activities in ventral and dorsal spinal cord were measured with ［3 H］-L-Arginine conversion. The iNOS mRAN expression and its cell distribution were detected with in situ hybridization.RESULTS:Intrathecal injection of dynorphin A1-17 (Dyn) 20 nmol induced permant paraplegia and delayed neuronal death.The iNOS mRNA expression began to increase at 2～3 h, peaked at 4 h and remained extensive at 24～48 h after Dyn spinal neurotoxicity, predominantly in glia cells and large motoneurons. The iNOS activities in ventral cord significantly increased at 4 h and persisted up to 24～48 h. Intrathecal pretreatment with aminoguanidine 1 μmol, a selective iNOS inhibitor, 10 min before Dyn 20 nmol significantly ameliorated Dyn-induced neurological outcome and antagonized the increase of iNOS activities at 4 h after Dyn neurotoxicity. CONCLUSION:Persistent high expression of iNOS might be involved in the pathophysiology of dynorphin-induced spina[1] [2] [3] 下一页
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