短暂性脑缺血后肿瘤坏死因子α（TNFα）的表达
Expression of tumor necrosis factor alpha (TNFalpha) following transient cerebral ischemia.
作者信息
Yin L, Ohtaki H, Nakamachi T, Dohi K, Iwai Y, Funahashi H, Makino R, Shioda S
机构信息
Department of Anatomy, Showa University School of Medicine, Tokyo, Japan.
出版信息
Acta Neurochir Suppl. 2003;86:93-6. doi: 10.1007/978-3-7091-0651-8_21.
It has been considered that tumor necrosis factor alpha (TNFalpha) is participated in the Alzheimer's, and Parkinson's diseases, brain injury and brain ischemia. However, expression of TNFalpha after brain ischemia has not been demonstrated in detail. Therefore we examined the cellular expression of TNFalpha during and after transient middle cerebral artery occlusion (tMCAO) in mice by use of reverse transcriptase-polymerase chain reaction and immunohistochemical technique. TNFalpha mRNA expression was gradually increased in the neocortex of the ipsilateral hemisphere during ischemia and peaked at 1 hour after reperfusion. Then, the mRNA expression decreased and peaked again at 24 hours after reperfusion. TNFalpha-like immunoreactivities were observed in the process such as dendrite of neuron slightly before ischemia, and markedly increased in neurons in addition to the process of the ipsilateral hemisphere at 1 and 24 hours after ischemia. The results suggest that the expression of TNFalpha is up-regulated in the neurons after tMCAO. TNFalpha may induce ischemic neuronal cell death during ischemic insult.
人们认为肿瘤坏死因子α（TNFα）与阿尔茨海默病、帕金森病、脑损伤和脑缺血有关。然而，脑缺血后TNFα的表达尚未得到详细证实。因此，我们通过逆转录-聚合酶链反应和免疫组织化学技术，研究了小鼠短暂性大脑中动脉闭塞（tMCAO）期间及之后TNFα的细胞表达情况。缺血期间，同侧半球新皮质中TNFα mRNA表达逐渐增加，并在再灌注后1小时达到峰值。然后，mRNA表达下降，并在再灌注后24小时再次达到峰值。在缺血前稍早时，在神经元树突等过程中观察到TNFα样免疫反应性，缺血后1小时和24小时，除同侧半球的过程外，神经元中的免疫反应性明显增加。结果表明，tMCAO后神经元中TNFα的表达上调。TNFα可能在缺血性损伤期间诱导缺血性神经元细胞死亡。
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