Morphine modulates chemokine gene regulation in normal human astrocytes
Morphine modulates chemokine gene regulation in normal human astrocytes
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DOI：
10.1016/j.clim.2005.02.004
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发表时间：
2005-06-01
影响因子：
8.6
通讯作者：
Nair, MPN
中科院分区：
文献类型：
--
作者：
Mahajan, SD;Schwartz, SA;Nair, MPN
趋化因子及其受体与神经艾滋病的发病机制有关。在此，我们描述了吗啡油对原代正常人星形胶质细胞 (NHA) β 趋化因子及其受体基因表达的影响。我们的结果表明，用吗啡处理的 NHA 显着下调 β 趋化因子、MCP-1 和 MIP-1 β 的基因表达，同时通过实时定量 PCR 检测到相应上调其特定受体 CCR2b、CCR3 和 CCR5 的表达。这些吗啡诱导的 NHA 细胞效应可被阿片类 mu 受体拮抗剂纳洛酮逆转。此外，我们的结果表明吗啡诱导的作用是通过调节 MAPK 和 CREB 信号通路介导的。这些结果支持我们的假设，即阿片类药物在 HIV 感染的神经发病机制中充当辅助因素。 (c) 2005 Elsevier Inc. 保留所有权利。
Chemokines and their receptors have been implicated in the pathogenesis of neuroAIDS. Herein we describe the effects of morphine oil the gene expression of beta chemokines and their receptors by primary normal human astrocytes (NHA). Our results show that NHA treated with morphine showed significant down regulation of the gene expression of beta chemokines, MCP-1, and MIP-1 beta, while reciprocally upregulating the expression of their specific receptors, CCR2b, CCR3, and CCR5 as detected by real-time quantitative PCR. These morphine-induced effects oil NHA cells were reversed by the opioid mu receptor antagonist, naloxone. Further, our results indicate that morphine-induced effects are mediated via the modulation of MAPK and CREB signaling pathways. These results support our hypothesis that opiates act as co-factors in the neuropathogenesis of HIV infection. (c) 2005 Elsevier Inc. All rights reserved.