Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats
Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats
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DOI：
10.1016/j.jneuroim.2005.04.025
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发表时间：
2005-08-01
影响因子：
3.3
通讯作者：
Beas-Zárate, C
中科院分区：
文献类型：
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作者：
Chaparro-Huerta, V;Rivera-Cervantes, MC;Beas-Zárate, C
促炎细胞因子tnf - α、IL-1 β和IL-6在神经元损伤期间升高，并激活凋亡的丝裂原活化蛋白激酶p38。我们研究了新生儿暴露于谷氨酸后8、10和14日龄大鼠的细胞凋亡、tnf - α、IL-1 β和IL-6水平以及产生tnf - α的细胞类型，谷氨酸诱导神经元损伤。谷氨酸显著增加tnf - α的产生，但被SB203580（一种p38抑制剂）抑制。tnf - α、IL-1 β和IL-6 mRNA水平升高，但SB203580未改变其表达。因此，p38信号通路影响炎症基因的表达，抑制其可能提供抗炎治疗。(C) 2005 Elsevier B.V.版权所有
The proinflammatory cytokines TNF-alpha, IL-1 beta, and IL-6 rise during neuronal damage and activate the apoptotic mitogen-activated protein kinase p38. We studied apoptosis, the levels of TNF-alpha, IL-1 beta, and IL-6, and the cell type producing TNF-alpha in rats at 8, 10, and 14 days of age after neonatal exposure to glutamate, which induces neuronal damage. TNF-alpha production was significantly increased by glutamate, but inhibited by SB203580 (a p38 inhibitor). TNF-alpha, IL-1 beta, and IL-6 mRNA levels increased, but SB203580 did not modify their expression. Thus, the p38 signaling pathway influences the expression of inflammatory genes and its inhibition may offer anti-inflammatory therapy. (C) 2005 Elsevier B.V. All rights reserved.