Bacterial endotoxin induces STAT3 activation in the mouse brain
Bacterial endotoxin induces STAT3 activation in the mouse brain
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DOI：
10.1016/j.brainres.2004.06.076
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发表时间：
2004-10-08
期刊：
影响因子：
2.9
通讯作者：
Nomura, Y
中科院分区：
文献类型：
--
作者：
Hosoi, T;Okuma, Y;Nomura, Y
在本研究中，我们研究了细菌内毒素诱导的STAT3激活在大脑中的调节机制。腹腔注射脂多糖（LPS）剂量依赖性（0.5-5000马克杯/千克）诱导下丘脑STAT3磷酸化。lps诱导的STAT3磷酸化在2-4 h达到峰值，随后下降。此外，脑室内注射LPS诱导皮层和海马STAT3磷酸化，表明中枢和外周LPS可以在大脑中作用诱导STAT3激活。已知糖皮质激素在内分泌系统免疫/炎症反应的反馈抑制中起生理作用。有趣的是，我们没有观察到地塞米松对lps诱导的下丘脑STAT3磷酸化的影响。这些发现指出了STAT3在大脑炎症的神经免疫相互作用中的重要作用。(C) 2004 Elsevier b.v.版权所有
In the present study, we investigated regulatory mechanisms of bacterial endotoxin-induced STAT3 activation in the brain. Intraperitoneal injection of lipopolysaccharide (LPS) dose-dependently (0.5-5000 mug/kg) induced STAT3 phosphorylation in the hypothalamus. LPS-induced STAT3 phosphorylation was peaked at 2-4 h and declined there after. Moreover, intracerebroventricular injection of LPS induced STAT3 phosphorylation in the cortex and the hippocampus, indicating that central as well as peripheral LPS can act in the brain to induce STAT3 activation. Glucocorticoids are known to play a physiological role in the feedback inhibition of immune/inflammatory responses in the endocrine system. Interestingly, we observed no effect of dexamethasone on LPS-induced STAT3 phosphorylation in the hypothalamus. These findings point to the important role of STAT3 in the neuroimmune interaction of inflammation in the brain. (C) 2004 Elsevier B.V All rights reserved.