小胶质细胞与缺血缺氧性脑损伤关系的研究进展

摘要
图/表
参考文献(37)
相关文章 (15)

全文: PDF (708 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要小胶质细胞是中枢神经系统的主要免疫细胞，其介导的炎性反应在缺血缺氧性脑损伤中起着重要的作用。缺血性卒中是脑血管病的常见类型，现有的治疗手段不能获得满意的临床疗效，因此研究小胶质细胞的作用机制对缺血性卒中的治疗具有重要意义。本文就近年来国内外关于小胶质细胞活化及其对缺血缺氧性脑损伤的作用、相关药物治疗等研究展开综述，为缺血性卒中的治疗提供新思路。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	刘波1 王嘉麟1 陈师林2 石静纹1 雷彬1 王一帆1 李红培1

关键词 ：小胶质细胞, 缺血缺氧性脑损伤, 炎性反应, 药物治疗

Abstract：Microglia cells is the main immune cells in the central nervous system, which induced inflammatory response plays an important role in ischemic-hypoxic brain injury. Ischemic stroke is a common type of cerebrovascular disease, and the existing treatment methods cannot achieve satisfactory clinical efficacy. Therefore, the study on the mechanism of action of microglia cells is of great significance for the treatment of ischemic stroke. In this paper, recent studies on microglia activation and its effect on ischemic and hypoxic brain injury and related drug therapy at home and abroad were reviewed, providing new ideas for the treatment of ischemic stroke.

Key words： Microglial cells Hypoxic-ischemic brain damage Inflammatory response Pharmaceutical drug

基金资助:国家中医药管理局国家中医临床研究基地业务建设科研专项课题（JDZX2015291）。

通讯作者: 王嘉麟（1982-），男，医学博士，副主任医师，硕士生导师；研究方向：中西医结合防治脑病基础与临床。

作者简介: 刘波（1992-），男，北京中医药大学东方医院2016级中医内科学（脑病）在读硕士研究生；研究方向：中西医结合防治脑病基础与临床。

引用本文:

刘波1 王嘉麟1 陈师林2 石静纹1 雷彬1 王一帆1 李红培1. 小胶质细胞与缺血缺氧性脑损伤关系的研究进展[J]. 中国医药导报, 2019, 16(9): 38-42.
LIU Bo1 WANG Jialin1 CHEN Shilin2 SHI Jingwen1 LEI Bin1 WANG Yifan1 LI Hongpei1. Research progress about the relationship between microglial cells and ischemic-hypoxic brain injury. 中国医药导报, 2019, 16(9): 38-42.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2019/V16/I9/38

[1] Hu X，Leak RK，Shi Y，et al. Microglial and macrophage polarization-new prospects for brain repair [J]. Nat Rev Neurol，2015，11（1）：56-64.
[2] Xiong XY，Liu L，Yang QW. Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke [J]. Prog Neurobiol，2016，142：23-44.
[3] Zhao S，Ma L，Chu Z，et al. Regulation of microglial activation in stroke [J]. Acta Pharmacol Sin，2017，38（4）：445-458.
[4] Lim JE，Chung E，Son Y. A neuropeptide，Substance-P，directly induces tissue-repairing M2 like macrophages by activating the PI3K/Akt/mTOR pathway even in the presence of IFNγ [J]. Sci Rep，2017，7（1）：9417.
[5] Han Q，Liu S，Li Z，et al. DCPIB，a potent volume-regulated anion channel antagonist，attenuates microglia-mediated inflammatory response and neuronal injury following focal cerebral ischemia [J]. Brain Res，2014，1542（2）：176-185.
[6] Cai Z，Zhao B，Deng Y，et al. Notch signaling in cerebrovascular diseases （Review） [J]. Mol Med Rep，2016，14（4）：2883-2898.
[7] Hu X，Li P，Guo Y，et al. Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia [J]. Stroke，2012，43（11）：3063-3070.
[8] Orihuela R，McPherson CA，Harry GJ. Microglial M1/M2 polarization and metabolic states [J]. Br J Pharmacol，2016， 173（4）：649-665.
[9] Sun W，Ding Z，Xu S，et al. Crosstalk between TLR2 and Sphk1 in microglia in the cerebral ischemia/reperfusion-induced inflammatory response [J]. Int J Mol Med，2017， 40（6）：1750-1758.
[10] Lambertsen KL，Biber K，Finsen B. Inflammatory cytokines in experimental and human stroke [J]. J Cereb Blood Flow Metab，2012，32（9）：1677-1698.
[11] Zhang Z，Qin P，Deng Y，et al. The novel estrogenic receptor GPR30 alleviates ischemic injury by inhibiting TLR4-mediated microglial inflammation [J]. J Neuroinflammation，2018，15（1）：206.
[12] Rempe RG，Hartz AM，Bauer B. Matrix metalloproteinases in the brain and blood-brain barrier：Versatile breakers and makers [J]. J Cereb Blood Flow Metab，2016，36（9）：1481-1507.
[13] Misra S，Talwar P，Kumar A，et al. Association between matrix metalloproteinase family gene polymorphisms and risk of ischemic stroke：A systematic review and meta-analysis of 29 studies [J]. Gene，2018，672：180-194.
[14] Chang JJ，Ansley S，Tayebeh P. The Role of Matrix Metalloproteinase Polymorphisms in Ischemic Stroke [J]. Int J Mol Sci，2016，17（8）：1323.
[15] Ma F，Martínez-San Segundo P，Barceló V，et al. Matrix metalloproteinase-13 participates in neuroprotection and neurorepair after cerebral ischemia in mice [J]. Neurobiol Dis，2016，91：236-246.
[16] 薛鑫，陈星星，王冠，等.甲酰基肽受体1对BV-2细胞迁移的影响及机制的体外研究[J].第三军医大学学报，2016，38（1）：44-49.
[17] Fung S，Cherry AE，Xu C，et al. Alkylindole-sensitive receptors modulate microglial cell migration and proliferation [J]. Glia，2015，63（10）：1797-1808.
[18] Sipe GO，Lowery RL，Tremblay Mè，et al. Microglial P2Y12 is necessary for synaptic plasticity in mouse visual cortex [J]. Nat Commun，2016，7：10905.
[19] Zhang F，Nance E，Alnasser Y，et al. Microglial migration and interactions with dendrimer nanoparticles are altered in the presence of neuroinflammation [J]. J Neuroinflammation，2016，13（1）：1-11.
[20] Charolidi N，Schilling T，Eder C. Microglial Kv1.3 Channels and P2Y12 Receptors Differentially Regulate Cytokine and Chemokine Release from Brain Slices of Young Adult and Aged Mice [J]. PLoS One，2015，10（5）：e0128463.
[21] Fu Y，Xin Z，Liu B，et al. Platycodin D Inhibits Inflammatory Response in LPS-Stimulated Primary Rat Microglia Cells through Activating LXRα-ABCA1 Signaling Pathway [J]. Front Immunol，2018，8：1929.
[22] Khan A，Ju F，Xie W，et al. Transcriptomic analysis reveals differential activation of microglial genes after ischemic strokein mice [J]. Neuroscience，2017，348：212-227.
[23] Fernández-López D，Faustino J，Klibanov AL，et al. Microglial Cells Prevent Hemorrhage in Neonatal Focal Arterial Stroke [J]. J Neurosci，2016，36（10）：2881-2893.
[24] Imai F，Suzuki H，Oda J，et al. Neuroprotective effect of exogenous microglia in global brain ischemia [J]. J Cereb Blood Flow Metab，2007，27（3）：488-500.
[25] Szalay G，Martinecz B，Lénárt N，et al. Microglia protect against brain injury and their selective elimination dysregulates neuronal network activity after stroke [J]. Nat Commun，2016，7：11499.
[26] Puig B，Brenna S，Magnus T. Molecular Communication of a Dying Neuron in Stroke [J]. Int J Mol Sci，2018，19（9）.pii：E2834.
[27] Yang Y，Liu H，Zhang H，et al. ST2/IL-33-Dependent Microglial Response Limits Acute Ischemic Brain Injury [J]. J Neurosci，2017，37（18）：4692-4704.
[28] Zhao X，Wang H，Sun G，et al. Neuronal Interleukin-4 as a Modulator of Microglial Pathways and Ischemic Brain Damage [J]. J Neurosci，2015，35（32）：11281-11291.
[29] Hong KS，Lee JS. Statins in Acute Ischemic Stroke：A Systematic Review [J]. J Stroke，2015，17（3）：282-301.
[30] Kata D，F?觟ldesi I，Feher LZ. Rosuvastatin enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells [J]. Neuroscience，2016，314：47-63.
[31] Zhou X，Cao Y，Ao G，et al. CaMKKβ-dependent activation of AMP-activated protein kinase is critical to suppressive effects of hydrogen sulfide on neuroinflammation [J]. Antioxid Redox Signal，2014，21（12）：1741-1758.
[32] Yuan Y，Zha H，Rangarajan P，et al. Anti-inflammatory effects of Edaravone and Scutellarin in activated microglia in experimentally induced ischemia injury in rats and in BV-2 microglia [J]. BMC Neurosci，2014，15（1）：1-21.
[33] Li F，Ma Q，Zhao H. L-3-n-Butylphthalide reduces ischemic stroke injury and increases M2 microglial polarization [J]. Metab Brain Dis，2018，33（6）：1995-2003.
[34] Patnala R，Arumugam TV，Gupta N，et al. HDAC Inhibitor Sodium Butyrate-Mediated Epigenetic Regulation Enhances Neuroprotective Function of Microglia During Ischemic Stroke [J]. Mol Neurobiol，2017，54（8）：6391-6411.
[35] Liu R，Diao J，He S，et al. XQ-1H protects against ischemic stroke by regulating microglia polarization through PPARγ pathway in mice [J]. Int Immunopharmacol，2018， 57：72-81.
[36] Liu X，Wen S，Yan F，et al. Salidroside provides neuroprotection by modulating microglial polarization after cerebral ischemia [J]. J Neuroinflammation，2018，15（1）：39.
[37] Zhou L，Zhang J，Wang C，et al. Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model [J]. Int J Immunopathol Pharmacol，2017，30（2）：123-129.