内源性大麻素系统对慢性脑低灌注患者认知功能障碍的调控作用

外科研究与新技术 ›› 2013, Vol. 2 ›› Issue (1): 41-44.

内源性大麻素系统对慢性脑低灌注患者认知功能障碍的调控作用

吴一芳, 余飞, 苏少华(综述), 海舰(审校)

同济大学附属同济医院神经外科, 上海 200065

出版日期:2013-03-28 发布日期:2013-01-25
通讯作者: 海舰,主任医师,博士生导师,研究脑血管疾病。 E-mail:haijiandoc@yahoo.com.cn
作者简介:吴一芳(1984-), 男, 江西人, 硕士在读, 研究脑缺血认识功能。
基金资助:
国家自然科学基金资助项目(81271212)

The regulatory effects of the endocannabinoid system on cognitive dysfunction in patient with chronic cerebral hypoperfusion

WU Yi-fang, YU Fei, SU Shao-hua, HAI Jian

Department of Neurosurgery,Tongji Hospital,Tongji University School of Medicine,Shanghai 200065, China

Online:2013-03-28 Published:2013-01-25

摘要/Abstract

摘要： 慢性脑低灌注诱导神经细胞变性,是导致患者认知功能障碍和社会能力低下的重要因素之一,脑血管疾病的病理发生有密切的关系。内源性大麻毒素(ECS)包括G蛋白耦联受体CB1、CB2,内源性配基AEA、2-AG及其内源性配基失活系统AEA水解酶FAAH等,国内外研究表明ECS在中枢神经系统具有多种内源性生理性调节作用并介导哺乳动物的神经保护作用,其主要表现在受体水平、失活系统、免疫应答及突触可塑性等方面;现就内源性大麻素系统(ECS)对慢性脑低灌注患者认知功能障碍的调控作用作一综述。

关键词: 内源性大麻素系统, 慢性脑低灌注, 认知功能障碍, 调控作用

Abstract: Chronic cerebral hypoperfusion induced degeneration of nerve cells is one of the important factors in low social ability in patients with cognitive dysfunction,and is closely linked to pathology of neurodegenerative and cerebrovascular disease.Domestic and foreign researches on Endocannabinoid toxin (ECS) including G protein-coupled receptor CB1,CB2,AEA,2-AG endogenous ligand and its endogenous ligand deactivation system AEA hydrolase FAAH have shown that ECS has a neuroprotective effect of endogenous physiological regulation mediated in mammalian central nervous system,which is mainly manifested in the receptor level,deactivation system,immune responses and synaptic plasticity and so on.This article is to review the endocannabinoid system (ECS) effects on cognitive impairment in patients with chronic cerebral hypoperfusion.

Key words: Endocannabinoid system, Chronic cerebral hypoperfusion, Cognition dysfunction, Regulate and control effect

中图分类号:

R742

吴一芳, 余飞, 苏少华, 海舰. 内源性大麻素系统对慢性脑低灌注患者认知功能障碍的调控作用[J]. 外科研究与新技术, 2013, 2(1): 41-44.

WU Yi-fang, YU Fei, SU Shao-hua, HAI Jian. The regulatory effects of the endocannabinoid system on cognitive dysfunction in patient with chronic cerebral hypoperfusion[J]. 外科研究与新技术, 2013, 2(1): 41-44.

参考文献

[1] Demuth DG,Mollema A.Cannabinoid signaling [J].Life Sci,2006,78(6):549-563.
[2] Bosier B,Muccioli GG,Hermans E,et al.Functionally selective cannabinoid receper signaling:therapeutic implications and opportunities[J].Biochem Pharmacol,2010,80(1):1-12.
[3] Tagliaferro P,Javier Ramos A,Onaivi ES,et al.Neuronal cytoskeleton and synaptic densities are altered after a chronic treatment with the cannabinoid receptor agonist WIN 55,212-2[J].Brain Res,2006,1085(1):163-176.
[4] Hill MN,Patel S Campolongo P,et al.Functional interactions Between stress and the endocannabinoid system:from synaptic signaling to behavioral output[J].J Neurosci,2010,30(45):14980-14986.
[5] Mechoulam R,Ben-Shabat S,Hanu L,et al.Identification of an endogenous 2-monoglyceride,present in canine gut,that binds to cannabinoid receptors.Biochem Pharmacol[J],1995,50(1):83-90.
[6] Hanu L,Abu-Lafi S,Fride E,et al.2-arachidonyl glyceryl ether,an endogenous agonist of the cannabinoid CB1 receptor[J].Proc Natl Acad Sci,2001,98(7):3662-3665.
[7] Micale V,Mazzola C,Drago F,et al.Endocannabinoids and neurodegenerative diseases[J].Pharmaco Res.2007,56(5):382-392.
[8] Tagliaferro P,Javier Ramos A Onaivi ES,et al.Neuronal cytoskeleton and synaptic densities are altered after a chronic treatment with the cannabinoid receptor agonist WIN 55,212-2[J].Brain Res,2006,1085(1):163-176.
[9] Cachope R,Mackie K,Triller A,et al.Potentiation of electrical and chemical synaptictransmission mediated by endocannabinoids[J].Neuron,2007,56(6):1034-1047.
[10] Hayakawa K,MishimK,Abe K,et a1.Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism[J].Neuroreport,2004,15(15):2381-2385.
[11] Mauler F,Miaendorf J,De Vry J,et al.Characterization of the diarylether sulfonylester(-)-(R)-3-(2-hydroxymethylindanyl-4-oxy)phenyl-4,4,4-trifluoro-l-sulf nate(BAY 38-7271) as a potent cannabinoid receptor agonia with neuroprotective properties[J].J Pharmacol Exp Ther,2002,302(1):359-368.
[12] Nagayama T,Sinor AD,Simon RP,et a1.Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures[J].J Neurosci,1999,19(8):2987-2995.
[13] Pellegrini-Giampietro DE,Mannaioni G.Post-ischemic brain damage:the endocannabinoid system in the mechanisms of neuronal death[J].FEBS J,2009,276(1):2-12.
[14] Wagner JA,Jarai Z,Batkai S et al.Hemodynamic effects of cannabinoids:coronary and cerebral vasodilation mediated by cannabinoid CB1 receptors[J].Eur J Pharmacol.2001,423(2-3):203-2l0.
[15] Ferraro L,Tomasini MC,Gessa GL,et a1.The Cannabinoid Receptor Agonist WIN55,212-2 Regulates Glutamate Transmission in Rat Cerebral Cortex:all In Vivo and In Vitro Study[J].Cerebral Cortex,2001,ll(8):728-733.
[16] Domenici MR,Azad SC,Marsicano G,et a1.Cannabinoid receptor type l Located on presynaptic terminals of principal neurons in the forebrain controls glutamatergic synaptic Transmission[J].J Neurosci.2006,26(21):5794-5799.
[17] Hillard CJ.Endocannabinoids and vascular function[J].J Pharmacol Exp Ther,2000,294(1):27-32.