新生大鼠海马中由p38丝裂原活化蛋白激酶介导的谷氨酸诱导的兴奋性毒性后的促炎细胞因子与细胞凋亡
Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats.
作者信息
Chaparro-Huerta V, Rivera-Cervantes M C, Flores-Soto M E, Gómez-Pinedo U, Beas-Zárate C
机构信息
Laboratorio de Neurobiología Molecular, División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Guadalajara, México.
出版信息
J Neuroimmunol. 2005 Aug;165(1-2):53-62. doi: 10.1016/j.jneuroim.2005.04.025.
The proinflammatory cytokines TNF-alpha, IL-1beta, 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-1beta, 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-1beta, 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.
促炎细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）在神经元损伤时升高，并激活凋亡性丝裂原活化蛋白激酶p38。我们研究了新生大鼠在出生后第8、10和14天暴露于谷氨酸（可诱导神经元损伤）后的细胞凋亡、TNF-α、IL-1β和IL-6水平，以及产生TNF-α的细胞类型。谷氨酸显著增加了TNF-α的产生，但被SB203580（一种p38抑制剂）抑制。TNF-α、IL-1β和IL-6的mRNA水平升高，但SB203580并未改变它们的表达。因此，p38信号通路影响炎症基因的表达，抑制该通路可能提供抗炎治疗。
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