Cytokines participate in neuronal death induced by trimethyltin in the rat hippocampus via type II glucocorticoid receptors
Cytokines participate in neuronal death induced by trimethyltin in the rat hippocampus via type II glucocorticoid receptors
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DOI：
10.1016/j.neures.2004.06.019
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发表时间：
2004-10-01
影响因子：
2.9
通讯作者：
Kato, N
中科院分区：
文献类型：
--
作者：
Liu, Y;Imai, H;Kato, N
我们研究了IL-1 α和IL-1 β在三甲基锡（TMT）诱导的海马损伤后反应性胶质增生中的作用。IL-1 α在TMT后第4天在小胶质细胞中表达较早，而IL-1 β在TMT后第14天在大肿胀胶质细胞中表达明显。IL-1 α和IL-1 β的免疫反应性都被星形胶质细胞标记物波形蛋白双重标记，但没有被小胶质细胞标记物OX-42标记。在TMT给药前，肾上腺切除术（ADX）可增强IL-1 α/β的表达。皮质酮（Corticosterone，CORT）或地塞米松（dexamethasone，DEX）的补充不仅可抵消ADX的作用，而且可部分逆转TMT诱导的IL-1 α/β表达增强。这些变化与TMT诱导的海马CA 3区锥体细胞神经元死亡一致。提示反应性星形胶质细胞表达的IL-1 α/β通过II型糖皮质激素受体参与TMT神经毒性。(C)2004年Elsevier爱尔兰有限公司和日本神经科学学会。All rights reserved.
We investigated the role of IL-1alpha and IL-1beta expressed in the reactive gliosis following hippocampal damage induced by trimethyltin (TMT). IL-1alpha immunoreactivity was expressed earlier in small glial cells on day 4 post-TMT, while IL-1beta expression was obvious in large swollen glial cells on day 14 post-TMT. Both IL-1alpha and IL-1beta immunoreactivities were double-labeled with astrocyte marker, vimentin, but not with a microglia marker, OX-42. The expression of both IL-1alpha/beta was enhanced by adrenalectomy (ADX) prior to TMT administration. Corticosterone (CORT) or dexamethasone (DEX) supplementation not only cancelled effects of ADX, but also partially reversed TMT-induced enhancement of IL-1alpha/beta expressions. These changes coincided with TMT-induced neuronal death in CA3 pyramidal cells of the hippocampus. It is suggested that IL-1alpha/beta expressed in reactive astrocytes participate in TMT neurotoxicity via type II glucocorticoid receptors. (C) 2004 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.