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脑溢安对血红蛋白损伤神经元神经生长因子和白细胞介素1β表达的影响
引用本文:贺又腾,黎杏群,等.脑溢安对血红蛋白损伤神经元神经生长因子和白细胞介素1β表达的影响[J].湖南医科大学学报,2001,26(1):26-30.
作者姓名:贺又腾  黎杏群
摘    要:目的:观察脑溢安对体外培养神经元血红蛋白损伤后的保护作用及神经生长因子与白细胞介素-1表达的影响。方法:以50umol/L^-1血红蛋白造成培养海马神经元损伤,运用活细胞计数、Northern杂交、酶联免疫检测神经元存活数量、神经生长因子与白细胞介素-1mRNA及其蛋白表达水平。结果:体外培养大鼠海马神经元在含2%牛血清的培养液中可存活5个月以上。加入50umol.L^-1血红蛋白培养24h神经元死亡率为38.5%。同时加入脑溢安药液能显著降低神经元死亡率。血红蛋白可引起培养神经元白细胞介素-1mRNA与蛋白表达水平显著升高及神经生长因子的短暂升高,脑溢安能降低白细胞介素-1表达,维持神经生长因子持续表达。结论:脑溢安对血红蛋白损伤神经元具有保护作用,其机理与调节神经元白细胞素-1表达,维持神经生长因子持续表达。结论:脑溢安对血红蛋白损伤神经元具有保护作用。其机理与调节神经元白细胞素-1、神经生长因子表达有关。

关 键 词:神经生长因子  脑缺血  白细胞介素-1β  中医药治疗  血红蛋白损伤

Effects of nao-yi-an on expressions of nerve growth factor and interleukin-1 beta following injury induced by hemoglobin in cultured hippocampal neurons]
S T He,X Q Li,H X Zhang.Effects of nao-yi-an on expressions of nerve growth factor and interleukin-1 beta following injury induced by hemoglobin in cultured hippocampal neurons][J].Bulletin of Hunan Medical University,2001,26(1):26-30.
Authors:S T He  X Q Li  H X Zhang
Institution:Institute of Combined Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha 410078.
Abstract:OBJECTIVE: To investigate the effects of Nao-yi-an (NYA) on protecting the cultured hippocampal neurons against the injury induced by hemoglobin (Hb) and modulating the expressions of nerve growth factor (NGF) and interleukin-1 beta (IL-1 beta) following Hb injury. METHODS: The experimental techniques of neuronal culture, alive cells count, Northern blotting, and enzymelinked immunosorbent assay (ELISA) were employed to detect the survival rate of cultured neurons, the expression level of NGF and IL-1 beta following Hb injury in cultured hippocampal neurons. RESULTS: 1. The hippocampal neurons survived for more than 5 months in Dulbecco's modified Eagle medium (DMEM) containing 2% bovine serum. 2. 38.5% cultured neurons were dead in Lock' s solution with 5 mmol.L-1 glucose containing 50 mumol.L-1 Hb. The rate of survival neurons was significantly increased by addition of decoction of NYA. 3. The expression of IL-1 beta was markedly increased at 1 h, 3 h, 6 h, and 12 h after Hb injury. The expression of NGF was temporarily increased. 4. The levels of IL-1 beta mRNA and protein were significantly decreased in NYA treated group, while the expression of NGF mRNA and protein was not reduced. CONCLUSION: NYA has the effects on increasing the neuronal survival, decreasing the expression of IL-1 beta, and maintaining the expression of NGF following Hb injury in cultured neurons.
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