细胞因子与帕金森病

谢涛, 杜冠华*

中国药学杂志 ›› 2014, Vol. 49 ›› Issue (20) : 1773-1777.

PDF(705 KB)
PDF(705 KB)
中国药学杂志 ›› 2014, Vol. 49 ›› Issue (20) : 1773-1777. DOI: 10.11669/cpj.2014.20.001
综述

细胞因子与帕金森病

  • 谢涛, 杜冠华*
作者信息 +

Cytokines and Parkinson's Disease

  • XIE Tao, DU Guan-hua*
Author information +
文章历史 +

摘要

目的 综述在帕金森病中相关细胞因子的作用,以期从细胞因子角度指导该疾病的治疗。方法 对近几年关于细胞因子在帕金森病中作用的文献进行查阅、分析、归纳和总结。结果与结论 细胞因子作为炎症介质参与了帕金森病,或通过促炎作用加重帕金森病的进展或通过抗炎减缓疾病的发生或通过保护神经细胞来抑制帕金森病。

Abstract

OBJECTIVE To review the role of cytokines played in Parkinson to direct the treatment of the disease from the prospective of cytokines.METHODS This paper had consulted, analysed, concluded and summarized research progress of the functions of cytokines in Parkinson's disease. RESUTLS AND XONCLUSION Cytokines, as inflammatory mediators, is involved in Parkinson.Some cytokines can contribute to the progress and development by playing the role of proinflammatory. Others,however, may play the role of anti-inflammatory to slow down the progress of PD or as a protective agent to against the disease.

关键词

帕金森病 / 多巴胺 / 细胞因子 / 炎症

Key words

Parkinson's disease / dopamine / cytokines / inflammatory

引用本文

导出引用
谢涛, 杜冠华*. 细胞因子与帕金森病[J]. 中国药学杂志, 2014, 49(20): 1773-1777 https://doi.org/10.11669/cpj.2014.20.001
XIE Tao, DU Guan-hua*. Cytokines and Parkinson's Disease[J]. Chinese Pharmaceutical Journal, 2014, 49(20): 1773-1777 https://doi.org/10.11669/cpj.2014.20.001
中图分类号: R965   

参考文献

[1] SCHAPIRA A H. Mitochondria in the aetiology and pathogenesis of Parkinson's disease[J]. Lancet Neurol, 2008, 7(1): 97-109.[2] COOKSON M R,VAN DER BRUG M. Cell systems and the toxic mechanism (s) of α-synuclein[J]. Exp Neurol, 2008, 209(1): 5-11.[3] YACOUBIAN T A,STANDAERT D G. Targets for neuroprotection in Parkinson's disease[J]. Biochim Biophys Acta, 2009, 1792(7): 676-687.[4] FRITSCH T, SMYTH K A, WALLENDAL M S, et al. Parkinson disease: Research update and clinical management[J]. South Med J, 2012, 105(12): 650-656.[5] PHANI S,LOIKE J D, PRZEDBORSKI S. Neurodegeneration and inflammation in Parkinson's disease[J]. Parkinson Relat Disord, 2012, 18 (1): 207-209.[6] KHANDELWAL P J, HERMAN A M, MOUSSA C E. Inflammation in the early stages of neurodegenerative pathology[J]. J Neuroimmunol, 2011, 238(1-2): 1-11.[7] NIRANJAN R. The Role of inflammatory and oxidative stress mechanisms in the pathogenesis of Parkinson's disease: Focus on astrocytes[J]. Molecular Neurobiol, 2013,17(3): 1-11.[8] DELEIDI M,GASSER T. The role of inflammation in sporadic and familial Parkinson's disease[J]. Cell Mol Life Sci, 2013, 70(22): 4259-4273.[9] POTT GODOY M C, TARELLI R, FERRARI C C, et al. Central and systemic IL-1 exacerbates neurodegeneration and motor symptoms in a model of Parkinson's disease[J]. Brain, 2008, 131(7): 1880-1894.[10] KIM H S,SUH Y H. Minocycline and neurodegenerative diseases[J]. Behav Brain Res, 2009, 196(2): 168-179.[11] CORBETT G T,ROY A,PAHAN K. Gemfibrozil, a lipid-lowering drug, upregulates IL-1 receptor antagonist in mouse cortical neurons: Implications for neuronal self-defense[J]. J Immunol, 2012, 189(2): 1002-1013.[12] LOFRUMENTO D D, NICOLARDI G, CIANCIULLI A, et al. Neuroprotective effects of resveratrol in an MPTP mouse model of Parkinson's-like disease: Possible role of SOCS-1 in reducing pro-inflammatory responses[J]. Innate Immun, 2014, 20(3): 249-260.[13] WANG X, CHEN S, MA G, et al. Involvement of proinflammatory factors, apoptosis, caspase-3 activation and Ca2+ disturbance in microglia activation-mediated dopaminergic cell degeneration[J]. Mech Ageing Dev, 2005, 126(12): 1241-1254.[14] HOFMANN K W, SCHUH A F S, SAUTE J, et al. Interleukin-6 serum levels in patients with Parkinson's disease[J]. Neurochem Res, 2009, 34(8): 1401-1404.[15] BICK R J, POINDEXTER B J, KOTT M M, et al. Cytokines disrupt intracellular patterns of Parkinson's disease-associated proteins alpha-synuclein, tau and ubiquitin in cultured glial cells[J]. Brain Res, 2008, 121(7): 203-212.[16] KLEGERIS A, GIASSON B I, ZHANG H, et al. Alpha-synuclein and its disease-causing mutants induce ICAM-1 and IL-6 in human astrocytes and astrocytoma cells[J]. FASEB J, 2006, 20(12): 2000-2008.[17] BEYNON A L, BROWN M R, WRIGHT R, et al. Ghrelin inhibits LPS-induced release of IL-6 from mouse dopaminergic neurones[J]. J Neuroinflam, 2013, 10(1): 40.[18] CHU K,ZHOU X,LUO B Y. Cytokine gene polymorphisms and Parkinson's disease: A meta-analysis[J]. Can J Neurol Sci, 2012, 39(1): 58-64.[19] RENTZOS M, NIKOLAOU C, ANDREADOU E, et al. Circulating interleukin-10 and interleukin-12 in Parkinson's disease[J]. Acta Neurol Scand, 2009, 119(5): 332-337.[20] JOHNSTON L C, SU X, MAGUIRE-ZEISS K, et al. Human interleukin-10 gene transfer is protective in a rat model of Parkinson's disease[J]. Mol Ther, 2008, 16(8): 1392-1399.[21] XIN J, WAINWRIGHT D A, MESNARD N A, et al. IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection[J]. Brain Behav Immun, 2011, 25(5): 820-829.[22] KUTER K, KOLASIEWICZ W, GOLEMBIOWSKA K, et al. Partial lesion of the dopaminergic innervation of the ventral striatum induces "depressive-like" behavior of rats[J]. Pharmacol Rep, 2011, 63(6): 1383-1392.[23] SCHWENKGRUB J, JONIEC-MACIEJAK I, SZNEJDER-PACHO LEK A, et al. Effect of human interleukin-10 on the expression of nitric oxide synthases in the MPTP-based model of Parkinson's disease[J]. Pharmacol Rep, 2013, 65(1): 44-49.[24] LI D, HE Q, LI R, et al. Interleukin-10 promoter polymorphisms in Chinese patients with Parkinson's disease[J]. Neurosci Lett, 2012, 513(2): 183-186.[25] RENTZOS M,ROMBOS A. The role of IL-15 in central nervous system disorders[J]. Acta Neurol Scand, 2012, 125(2): 77-82.[26] MEUER K, PITZER C, TEISMANN P, et al. Granulocyte-colony stimulating factor is neuroprotective in a model of Parkinson's disease[J]. J Neurochem, 2006, 97(3): 675-686.[27] LIAO C H, CHEN S Y, KUO J S, et al. Reduction of motor disorder in 6-OHDA-induced severe parkinsonism rats by post treatment with granulocyte-colony stimulating factor[J]. Chin J Physiol(中国生理学报), 2013, 56(3): 147-154.[28] SONG S, SAVA V, ROWE A, et al. Granulocyte-colony stimulating factor (G-CSF) enhances recovery in mouse model of Parkinson's disease[J]. Neurosci Lett, 2011, 487(2): 153-157.[29] MEUER K, PITZER C, TEISMANN P, et al. Granulocyte-colony stimulating factor is neuroprotective in a model of Parkinson's disease[J]. J Neurochem, 2006, 97(3): 675-686.[30] SCHNEIDER A, KRUGER C, STEIGLEDER T, et al. The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis[J]. J Clin Invest, 2005, 115(8): 2083-2098.[31] HENZE C, HARTMANN A, LESCOT T, et al. Proliferation of microglial cells induced by 1-methyl-4-phenylpyridinium in mesencephalic cultures results from an astrocyte-dependent mechanism: Role of granulocyte macrophage colony-stimulating factor[J]. J Neurochem, 2005, 95(4): 1069-1077.[32] SCHABITZ W R, KRUGER C, PITZER C, et al. A neuroprotective function for the hematopoietic protein granulocyte-macrophage colony stimulating factor (GM-CSF)[J]. J Cereb Blood Flow Metab, 2008, 28(1): 29-43.[33] KIM N K, CHOI B H, HUANG X, et al. Granulocyte-macrophage colony-stimulating factor promotes survival of dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced murine Parkinson's disease model[J]. Eur J Neurosci, 2009, 29(5): 891-900.[34] MANGANO E N, PETERS S, LITTELJOHN D, et al. Granulocyte macrophage-colony stimulating factor protects against substantia nigra dopaminergic cell loss in an environmental toxin model of Parkinson's disease[J]. Neurobiol Dis, 2011, 43(1): 99-112.[35] CHOUDHURY M E, SUGIMOTO K, KUBO M, et al. A cytokine mixture of GM-CSF and IL-3 that induces a neuroprotective phenotype of microglia leading to amelioration of (6-OHDA)-induced Parkinsonism of rats[J]. Brain Behav, 2011, 1(1): 26-43.[36] KOSLOSKI L M, KOSMACEK E A, OLSON K E, et al. GM-CSF induces neuroprotective and anti-inflammatory responses in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine intoxicated mice[J]. J Neuroimmunol, 2013, 265(1-2): 1-10.[37] WHITTON P S. Inflammation as a causative factor in the aetiology of Parkinson's disease[J]. Br J Pharmacol, 2007, 150(8): 963-976.[38] HARMS A S, BARNUM C J, RUHN K A, et al. Delayed dominant-negative TNF gene therapy halts progressive loss of nigral dopaminergic neurons in a rat model of Parkinson's disease[J]. Mol Ther, 2011, 19(1): 46-52.[39] BIALECKA M, KLODOWSKA-DUDA G, KURZAWSKI M, et al. Interleukin-10(IL-10) and tumor necrosis factor alpha (TNF) gene polymorphisms in Parkinson's disease patients[J]. Parkinson Relat Disord, 2008, 14(8): 636-640.[40] HIRSCH E C,HUNOT S. Neuroinflammation in Parkinson's disease: A target for neuroprotection[J]. Lancet Neurol, 2009, 8(4): 382-397.[41] AL-AMRI J S,HAGRAS M M,MOHAMED I M. Effect of epigallocatechin-3-gallate on inflammatory mediators release in LPS-induced Parkinson's disease in rats[J]. Indian J Exp Biol, 2013, 51(5): 357-362.[42] PETERSON A L,NUTT J G. Treatment of Parkinson's disease with trophic factors[J]. Neurotherapeutics, 2008, 5(2): 270-280.[43] BAQUET Z C,BICKFORD P C,JONES K R. Brain-derived neurotrophic factor is required for the establishment of the proper number of dopaminergic neurons in the substantia nigra pars compacta[J]. J Neurosci, 2005, 25(26): 6251-6259.[44] VON BOHLEN UND HALBACH O,MINICHIELLO L,UNSICKER K. Haploinsufficiency for trkB and trkC receptors induces cell loss and accumulation of alpha-synuclein in the substantia nigra[J]. FASEB J, 2005, 19(12): 1740-1742.[45] KORDOWER J H, HERZOG C D, DASS B, et al. Delivery of neurturin by AAV2 (CERE-120)-mediated gene transfer provides structural and functional neuroprotection and neurorestoration in MPTP-treated monkeys[J]. Ann Neurol, 2006, 60(6): 706-715.[46] HERZOG C D, DASS B, HOLDEN J E, et al. Striatal delivery of CERE-120, an AAV2 vector encoding human neurturin, enhances activity of the dopaminergic nigrostriatal system in aged monkeys[J]. Mov Disord, 2007, 22(8): 1124-1132.

基金

国家“重大新药创制”科技重大专项(2013ZX09102106)
PDF(705 KB)

Accesses

Citation

Detail

段落导航
相关文章

/