Extracellular signal-regulated kinase-mediated IL-1-induced cortical neuron damage during traumatic brain injury

Kwok Tung Lu, Yi Wen Wang, Yu Yuan P. Wo, Yi Ling Yang*

*此作品的通信作者

研究成果: 雜誌貢獻期刊論文同行評審

66 引文 斯高帕斯(Scopus)

摘要

Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity and mortality in youth. Interleukin-1 (IL-1) has many roles in the brain in addition to mediating glial inflammatory response; it has also been implicated in neurodegenerative diseases. We demonstrated the signal transduction pathway of IL-1 overproduction-induced cortical neuron loss during TBI. A calibrated weight-drop device (450 g weight and 2 m height) was used to induce TBI in adult male Sprague-Dawley rats under general anesthesia (sodium pentobarbital: 40 mg/kg, i.p.). Expression of interleukin-1α (IL-1α), interleukin-1β (IL-1β), extracellular signal-regulated kinase (ERK), Jun, and p-38 were determined by Western blotting and RT-PCR. Neuronal damage was evaluated by microscopic examination. We found both mRNA and proteins of cortical IL-1α and IL-1β increased three hours after TBI. Phosphorylation of ERK significantly increased but there were no significant effects on cortical expression of ERK, Jun and p-38. Administration of ERK inhibitor, PD98059, IL-1α antibody and IL-1β antibody protected animals from TBI-induced neuronal damage. Our results suggest that TBI-induced cortical neuron death was mediated by the IL-1 receptor through ERK phosphorylation.

原文英語
頁(從 - 到)40-45
頁數6
期刊Neuroscience Letters
386
發行號1
DOIs
出版狀態已發佈 - 2005 9月 23

ASJC Scopus subject areas

  • 一般神經科學

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