β-adrenoceptor mediated surgery-induced production of pro-inflammatory cytokines in rat microglia cells
β-adrenoceptor mediated surgery-induced production of pro-inflammatory cytokines in rat microglia cells
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DOI：
10.1016/j.jneuroim.2010.04.006
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发表时间：
2010-06-01
影响因子：
3.3
通讯作者：
Wu, Gen-Cheng
中科院分区：
文献类型：
--
作者：
Wang, Jun;Li, Jing;Wu, Gen-Cheng
大手术损伤引起的免疫改变可引起周围和中枢神经系统的炎症反应，从而导致器官功能障碍。最近的研究表明，β -肾上腺素能受体（β - ars）可能介导大脑中促炎细胞因子的产生。在目前的研究中，心得安（β - ar拮抗剂），而不是吡唑嗪（α - 1-AR拮抗剂），拮抗手术创伤诱导的大鼠分离的小胶质细胞中促炎细胞因子的产生。在没有促炎刺激的情况下，β - ar激活增加了原代小胶质细胞培养中IL-1 β、tnf - α和IL-6 mRNA和蛋白的表达。异丙肾上腺素（β - ar激动剂）处理诱导细胞中IL-1 β的时间和浓度依赖性增加。ERK1/2和P38 MAPK抑制剂，而不是PKA和JNK1/2抑制剂，都能消除异丙肾上腺素诱导的小胶质细胞中IL-1 β和IL-6的产生。综上所述，β - ar通过调节小胶质细胞的功能而具有促炎特性。(C) 2010 Elsevier B.V.版权所有
Immunological changes initiated by major operative injury may result in inflammatory responses in both peripheral and central nervous system, which may lead to organ dysfunction. Recent studies indicate that beta-adrenergic receptors (beta-ARs) may mediate production of pro-inflammatory cytokines in the brain. In the present study propranolol (beta-AR antagonist), but not prazosin (alpha 1-AR antagonist), antagonized surgical trauma induced pro-inflammatory cytokine production in microglia cells isolated from rats. beta-AR activation in the absence of pro-inflammatory stimuli increased IL-1 beta, TNF-alpha and IL-6 mRNA and protein expressions in the primary microglia cell culture. Isoproterenol (beta-AR agonist) treatment induced a time- and concentration-dependent increase of IL-1 beta in cells. Both ERK1/2 and P38 MAPK inhibitor, but not PKA and JNK1/2 inhibitor abrogated isoproterenol-induced IL-1 beta and IL-6 production in microglia cells. In conclusion, the results suggest that beta-ARs possess pro-inflammatory properties by modulating the functions of microglia cell. (C) 2010 Elsevier B.V. All rights reserved.