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本文引用的文献

1
Progesterone and estrogen regulate Alzheimer-like neuropathology in female 3xTg-AD mice.孕酮和雌激素调节雌性3xTg-AD小鼠的阿尔茨海默氏症样神经病理学。
J Neurosci. 2007 Nov 28;27(48):13357-65. doi: 10.1523/JNEUROSCI.2718-07.2007.
2
Nonsteroidal anti-inflammatory drugs may protect against Parkinson disease.非甾体抗炎药可能预防帕金森病。
Neurology. 2007 Nov 6;69(19):1836-42. doi: 10.1212/01.wnl.0000279519.99344.ad.
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The origin and application of experimental autoimmune encephalomyelitis.实验性自身免疫性脑脊髓炎的起源与应用
Nat Rev Immunol. 2007 Nov;7(11):904-12. doi: 10.1038/nri2190.
4
Differential neuroprotective and antiinflammatory effects of estrogen receptor (ER)alpha and ERbeta ligand treatment.雌激素受体(ER)α和ERβ配体治疗的差异性神经保护和抗炎作用
Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14813-8. doi: 10.1073/pnas.0703783104. Epub 2007 Sep 4.
5
Estrogen and CD4+ T cells.雌激素与CD4+ T细胞。
Curr Opin Rheumatol. 2007 Sep;19(5):414-20. doi: 10.1097/BOR.0b013e328277ef2a.
6
Increased risk of cognitive impairment or dementia in women who underwent oophorectomy before menopause.绝经前接受卵巢切除术的女性患认知障碍或痴呆的风险增加。
Neurology. 2007 Sep 11;69(11):1074-83. doi: 10.1212/01.wnl.0000276984.19542.e6. Epub 2007 Aug 29.
7
Neuroinflammation in Alzheimer's disease and Parkinson's disease: are microglia pathogenic in either disorder?阿尔茨海默病和帕金森病中的神经炎症:小胶质细胞在这两种疾病中都具有致病性吗?
Int Rev Neurobiol. 2007;82:235-46. doi: 10.1016/S0074-7742(07)82012-5.
8
MAC1 mediates LPS-induced production of superoxide by microglia: the role of pattern recognition receptors in dopaminergic neurotoxicity.MAC1介导小胶质细胞中脂多糖诱导的超氧化物生成:模式识别受体在多巴胺能神经毒性中的作用。
Glia. 2007 Oct;55(13):1362-73. doi: 10.1002/glia.20545.
9
Induction of regulatory T cells by physiological level estrogen.生理水平雌激素对调节性T细胞的诱导作用。
J Cell Physiol. 2008 Feb;214(2):456-64. doi: 10.1002/jcp.21221.
10
Microglial PHOX and Mac-1 are essential to the enhanced dopaminergic neurodegeneration elicited by A30P and A53T mutant alpha-synuclein.小胶质细胞的吞噬氧化酶(PHOX)和巨噬细胞抗原-1(Mac-1)对于由A30P和A53T突变型α-突触核蛋白引发的多巴胺能神经元变性增强至关重要。
Glia. 2007 Aug 15;55(11):1178-88. doi: 10.1002/glia.20532.

雌激素在大脑中的抗炎活性:绝经和神经退行性疾病的治疗契机。

Estrogen anti-inflammatory activity in brain: a therapeutic opportunity for menopause and neurodegenerative diseases.

作者信息

Vegeto Elisabetta, Benedusi Valeria, Maggi Adriana

机构信息

Centre of Excellence on Neurodegenerative Disease, University of Milan, via Balzaretti, 9 20133 Milan, Italy.

出版信息

Front Neuroendocrinol. 2008 Oct;29(4):507-19. doi: 10.1016/j.yfrne.2008.04.001. Epub 2008 Apr 29.

DOI:10.1016/j.yfrne.2008.04.001
PMID:18522863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2630539/
Abstract

Recent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

摘要

最近的研究突出了雌激素在保护中枢神经系统(CNS)免受慢性炎症反应有害后果方面所起的重要作用。包括多发性硬化症、阿尔茨海默病和帕金森病在内的几种中枢神经系统疾病的神经退行性过程与小胶质细胞的激活有关,小胶质细胞驱动局部炎症反应。在神经退行性变过程中受到长期刺激的小胶质细胞被认为会对周围神经元产生有害影响。因此,雌激素对神经炎症尤其是对小胶质细胞的抑制活性可能被视为延缓神经退行性疾病发病或进展的有益治疗机会;此外,了解这种女性激素在炎症信号通路中的特殊活性可能会导致开发特定的抗炎分子。本综述总结了小胶质细胞参与神经炎症的证据以及雌激素特别是在小胶质细胞中发挥的抗炎活性。