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Role of microglia in methamphetamine-induced neurotoxicity.小胶质细胞在甲基苯丙胺诱导的神经毒性中的作用。
Int J Physiol Pathophysiol Pharmacol. 2017 Jun 15;9(3):84-100. eCollection 2017.
2
Methamphetamine potentiates HIV-1gp120-induced microglial neurotoxic activity by enhancing microglial outward K current.甲基苯丙胺通过增强小胶质细胞外向钾电流来增强HIV-1 gp120诱导的小胶质细胞神经毒性活性。
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Methamphetamine enhancement of HIV-1 gp120-mediated NLRP3 inflammasome activation and resultant proinflammatory responses in rat microglial cultures.甲基苯丙胺增强HIV-1 gp120介导的大鼠小胶质细胞培养物中NLRP3炎性小体激活及由此产生的促炎反应。
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Inflammasome Activation by Methamphetamine Potentiates Lipopolysaccharide Stimulation of IL-1β Production in Microglia.甲基苯丙胺激活炎症小体增强脂多糖刺激小胶质细胞产生白细胞介素-1β。
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Methamphetamine neurotoxicity, microglia, and neuroinflammation.甲基苯丙胺神经毒性、小胶质细胞与神经炎症。
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Triggering Receptor Expressed on Myeloid Cells 2 Deficiency Exacerbates Methamphetamine-Induced Activation of Microglia and Neuroinflammation.髓系细胞表达的触发受体 2 缺陷加剧了甲基苯丙胺诱导的小胶质细胞激活和神经炎症。
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Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation.甲基苯丙胺诱导的神经元损伤:神经毒性与神经炎症
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Methamphetamine Enhancement of HIV-1 gp120-Mediated NLRP3 Inflammasome Activation and Resultant Proinflammatory Responses in Rat Microglial Cultures.甲基苯丙胺增强 HIV-1 gp120 介导体细胞焦亡小体激活和大鼠小胶质细胞培养物中随后的促炎反应。
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SN79, a sigma receptor ligand, blocks methamphetamine-induced microglial activation and cytokine upregulation.SN79,一种 sigma 受体配体,可阻断安非他命引起的小胶质细胞激活和细胞因子上调。
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Methamphetamine and HIV-1 Tat proteins synergistically induce microglial autophagy via activation of the Nrf2/NQO1/HO-1 signal pathway.甲基苯丙胺和 HIV-1 Tat 蛋白通过激活 Nrf2/NQO1/HO-1 信号通路协同诱导小胶质细胞自噬。
Neuropharmacology. 2022 Dec 1;220:109256. doi: 10.1016/j.neuropharm.2022.109256. Epub 2022 Sep 24.

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Ibudilast-Mediated Suppression of Neuronal TLR4 in the Prefrontal Cortex Mitigates Methamphetamine-Induced Neuroinflammation and Addictive Behaviours.异丁司特介导的前额叶皮质神经元Toll样受体4抑制减轻甲基苯丙胺诱导的神经炎症和成瘾行为。
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Methamphetamine-Induced Blood Pressure Sensitization Correlates with Morphological Alterations within A1/C1 Catecholamine Neurons.甲基苯丙胺诱导的血压敏化与 A1/C1 儿茶酚胺神经元的形态改变相关。
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6
Methamphetamine enhancement of HIV-1 gp120-mediated NLRP3 inflammasome activation and resultant proinflammatory responses in rat microglial cultures.甲基苯丙胺增强HIV-1 gp120介导的大鼠小胶质细胞培养物中NLRP3炎性小体激活及由此产生的促炎反应。
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Nanowired Delivery of Mesenchymal Stem Cells with Antioxidant Compound H-290/51 Reduces Exacerbation of Methamphetamine Neurotoxicity in Hot Environment.纳米载体递送间充质干细胞与抗氧化化合物 H-290/51 可减轻热环境中甲基苯丙胺神经毒性的恶化。
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Gut Microbiota Taxon-Dependent Transformation of Microglial M1/M2 Phenotypes Underlying Mechanisms of Spatial Learning and Memory Impairment after Chronic Methamphetamine Exposure.慢性甲基苯丙胺暴露后空间学习记忆损伤的潜在机制:肠道微生物群分类群依赖性小胶质细胞 M1/M2 表型转化。
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NRF2 Antagonizes HIV-1 Tat and Methamphetamine-Induced BV2 Cell Ferroptosis by Regulating SLC7A11.NRF2 通过调节 SLC7A11 拮抗 HIV-1 Tat 和冰毒诱导的 BV2 细胞铁死亡。
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Cognitive impairment and changes of red blood cell components and serum levels of IL-6, IL-18, and L-tryptophan in methamphetamine abusers.甲基苯丙胺滥用者的认知障碍以及红细胞成分和血清白细胞介素-6、白细胞介素-18和L-色氨酸水平的变化
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本文引用的文献

1
Molecular Mechanisms Involving Sigma-1 Receptor in Cell Apoptosis of BV-2 Microglial Cells Induced by Methamphetamine.甲基苯丙胺诱导BV-2小胶质细胞凋亡中涉及σ-1受体的分子机制
CNS Neurol Disord Drug Targets. 2016;15(7):857-65. doi: 10.2174/1871527315666160518122816.
2
Methamphetamine abuse affects gene expression in brain-derived microglia of SIV-infected macaques to enhance inflammation and promote virus targets.甲基苯丙胺滥用会影响感染猴免疫缺陷病毒(SIV)的猕猴脑源性小胶质细胞中的基因表达,从而增强炎症反应并促进病毒靶向作用。
BMC Immunol. 2016 Apr 23;17(1):7. doi: 10.1186/s12865-016-0145-0.
3
Potential Molecular Mechanisms on the Role of the Sigma-1 Receptor in the Action of Cocaine and Methamphetamine.西格玛-1受体在可卡因和甲基苯丙胺作用中的潜在分子机制
J Drug Alcohol Res. 2016 Feb 20;5. doi: 10.4303/jdar/235970.
4
Ibudilast attenuates subjective effects of methamphetamine in a placebo-controlled inpatient study.在一项安慰剂对照的住院患者研究中,异丁司特减轻了甲基苯丙胺的主观效应。
Drug Alcohol Depend. 2016 May 1;162:245-50. doi: 10.1016/j.drugalcdep.2016.02.036. Epub 2016 Mar 3.
5
The Role of Ion Channels in Microglial Activation and Proliferation - A Complex Interplay between Ligand-Gated Ion Channels, K(+) Channels, and Intracellular Ca(2.).离子通道在小胶质细胞激活和增殖中的作用——配体门控离子通道、钾离子通道和细胞内钙离子之间的复杂相互作用
Front Immunol. 2015 Oct 22;6:497. doi: 10.3389/fimmu.2015.00497. eCollection 2015.
6
The cross-talk of HIV-1 Tat and methamphetamine in HIV-associated neurocognitive disorders.HIV-1反式激活蛋白(Tat)与甲基苯丙胺在HIV相关神经认知障碍中的相互作用
Front Microbiol. 2015 Oct 23;6:1164. doi: 10.3389/fmicb.2015.01164. eCollection 2015.
7
Characterization of binge-dosed methamphetamine-induced neurotoxicity and neuroinflammation.大剂量甲基苯丙胺诱导的神经毒性和神经炎症的特征
Neurotoxicology. 2015 Sep;50:131-41. doi: 10.1016/j.neuro.2015.08.006. Epub 2015 Aug 15.
8
The danger-associated molecular pattern HMGB1 mediates the neuroinflammatory effects of methamphetamine.与危险相关的分子模式高迁移率族蛋白B1介导甲基苯丙胺的神经炎症效应。
Brain Behav Immun. 2016 Jan;51:99-108. doi: 10.1016/j.bbi.2015.08.001. Epub 2015 Aug 4.
9
The blood-brain barrier and methamphetamine: open sesame?血脑屏障与甲基苯丙胺:芝麻开门?
Front Neurosci. 2015 May 5;9:156. doi: 10.3389/fnins.2015.00156. eCollection 2015.
10
Ibudilast reverses the decrease in the synaptic signaling protein phosphatidylethanolamine-binding protein 1 (PEBP1) produced by chronic methamphetamine intake in rats.异丁司特可逆转大鼠长期摄入甲基苯丙胺所导致的突触信号蛋白磷脂酰乙醇胺结合蛋白1(PEBP1)的减少。
Drug Alcohol Depend. 2015 Jul 1;152:15-23. doi: 10.1016/j.drugalcdep.2015.04.012. Epub 2015 Apr 30.

小胶质细胞在甲基苯丙胺诱导的神经毒性中的作用。

Role of microglia in methamphetamine-induced neurotoxicity.

作者信息

Xu Enquan, Liu Jianuo, Liu Han, Wang Xiaobei, Xiong Huangui

机构信息

Neurophysiology Laboratory, Departments of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center Omaha 68198-5880, NE, USA.

College of Pharmacy, University of Nebraska Medical Center Omaha 68198-6125, NE, USA.

出版信息

Int J Physiol Pathophysiol Pharmacol. 2017 Jun 15;9(3):84-100. eCollection 2017.

PMID:28694920
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5498881/
Abstract

Methamphetamine (Meth) is an addictive psychostimulant widely abused around the world. The chronic use of Meth produces neurotoxicity featured by dopaminergic terminal damage and microgliosis, resulting in serious neurological and behavioral consequences. Ample evidence indicate that Meth causes microglial activation and resultant secretion of pro-inflammatory molecules leading to neural injury. However, the mechanisms underlying Meth-induced microglial activation remain to be determined. In this review, we attempt to address the effects of Meth on human immunodeficiency virus (HIV)-associated microglia activation both and . Meth abuse not only increases HIV transmission but also exacerbates progression of HIV-associated neurocognitive disorders (HAND) through activation of microglia. In addition, the therapeutic potential of anti-inflammatory drugs on ameliorating Meth-induced microglia activation and resultant neuronal injury is discussed.

摘要

甲基苯丙胺(冰毒)是一种成瘾性精神兴奋剂,在全球范围内被广泛滥用。长期使用冰毒会产生以多巴胺能终末损伤和小胶质细胞增生为特征的神经毒性,导致严重的神经和行为后果。大量证据表明,冰毒会导致小胶质细胞活化并分泌促炎分子,从而导致神经损伤。然而,冰毒诱导小胶质细胞活化的机制仍有待确定。在本综述中,我们试图探讨冰毒对人类免疫缺陷病毒(HIV)相关小胶质细胞活化的影响。滥用冰毒不仅会增加HIV传播,还会通过激活小胶质细胞加剧HIV相关神经认知障碍(HAND)的进展。此外,还讨论了抗炎药物在改善冰毒诱导的小胶质细胞活化及由此导致的神经元损伤方面的治疗潜力。