外源性二磷酸果糖在脑组织损伤中的保护作用
详细信息    查看全文 | 推荐本文 |
  • 英文篇名:Effect of Exogenous Fructose 1,6-Diphosphate on Neuroprotection
  • 作者:乔瑞峰 ; 汪明慧 ; 解旭东
  • 英文作者:QIAO Ruifeng;WANG Minghui;XIE Xundong;Medical Training Center of Army General Hospital;Department of Outpatient,Xicheng District NO.1 Retired Cadre Rehabilitation Center of Beijing Garrison;Department of Neurology,PLA NO.252 Hospital;
  • 关键词:1 ; 6-二磷酸果糖 ; 脑损伤 ; 脑保护 ; 药动学 ; 不良反应
  • 英文关键词:Fructose 1,6-diphosphate;;Cerebral injury;;Cerebral protection;;Pharmacokinetics;;Adverse reactions
  • 中文刊名:YXZS
  • 英文刊名:Medical Recapitulate
  • 机构:陆军总医院卫生干部训练中心;北京卫戍区西城第一离职干部休养所门诊部;解放军第二五二医院神经内科;
  • 出版日期:2019-03-22 08:40
  • 出版单位:医学综述
  • 年:2019
  • 期:v.25
  • 语种:中文;
  • 页:YXZS201906011
  • 页数:6
  • CN:06
  • ISSN:11-3553/R
  • 分类号:65-70
摘要
1,6-二磷酸果糖(FDP)在糖的无氧代谢过程中具有重要作用。给予人或动物外源性FDP后,其可迅速通过血脑屏障,被脑组织吸收利用,通过改善无氧糖酵解效率、维护细胞膜和溶酶体膜的稳定性、调节细胞内钙离子含量、改变离子通道的活性等机制,在脑缺血、一氧化碳中毒、惊厥、癫痫等脑部病变中发挥积极的脑保护作用。同时外源性FDP又具有不良反应少、配伍禁忌少、给药途径多、适用人群广泛等优点,具有较为广泛的临床应用前景。
        Fructose 1,6-diphosphate( FDP) has important roles in the process of intracellular glycolysis. After exogenous FDP is given to person or animal,it can get through the blood-brain barrier rapidly,and be absorbed and utilized by brain tissue. By the mechanisms such as improving anaerobic glycolysis efficiency,protecting the stability of cell membrane and lysosome membrane,regulating intracellular Ca~(2+) concentration and changing the ion channel activity,exogenous FDP has significant neuroprotection in the cerebral injuries,such as cerebral ischemia,carbon monoxide poisoning and epilepsy.Exogenous FDP has the characteristics of low adverse effect,less contraindication,multiple administration paths and wide applicability,so it has extensive clinical applicative prospect.
引文
[1]Zhang CS,Hawley SA,Zong Y,et al.Fructose-1,6-bisphosphate and aldolase mediate glucose sensing by AMPK[J].Nature,2017,548(7665):112-116.
    [2]Shams F,Oldfield NJ,Wooldridge KG,et al.Fructose-1,6-bisphosphate aldolase(FBA)-a conserved glycolytic enzyme with virulence functions in bacteria:Ill met by moonlight[J].Biochem Soc Trans,2014,42(6):1792-1795.
    [3]Murakami K,Yoshino M.Effect of fructose 1,6-bisphosphate on the iron redox state relating to the generation of reactive oxygen species[J].Biometals,2015,28(4):687-691.
    [4]Wang W,Liu M,You C,et al.ATP-free biosynthesis of a highenergy phosphate metabolite fructose 1,6-diphosphate by in vitro metabolic engineering[J].Metab Eng,2017,42:168-174.
    [5]Gregory GA,Yu AC,Chan PH.Fructose-1,6-bisphosphate protects astrocytes from hypoxic damage[J].J Cereb Blood Flow Metab,1989,9(1):29-34.
    [6]Alva N,Alva R,Carbonell T.Fructose 1,6-bisphosphate:A summary of its cytoprotective mechanism[J].Curr Med Chem,2016,23(39):4396-4417.
    [7]Barik S.How universal is the transcription regulatory moonlighting role of fructose 1,6-bisphosphate aldolase?[J].J Theor Biol,2018,464:112-114.
    [8]Li TT,Xie JZ,Wang L,et al.Rational application of fructose-1,6-diphosphate:From the perspective of pharmacokinetics[J].Acta Pharm,2015,65(2):147-157.
    [9]Stocchetti N,Taccone FS,Citerio G.Neuroprotection in acute brain injury:An up-to-date review[J].Crit Care,2015,19:186.
    [10]Mares J,Nohejlova K,Stopka P,et al.Direct measurement of free radical levels in the brain after cortical ischemia induced by photothrombosis[J].Physiol Res,2016,65(5):853-860.
    [11]Zhou F,Liu Y,Yang B,et al.Neuroprotective potential of glibenclamide is mediated by antioxidant and anti-apoptotic pathways in intracerebral hemorrhage[J].Brain Res Bull,2018,142:18-24.
    [12]Prins M,Greco T,Alexander D,et al.The pathophysiology of traumatic brain injury at a glance[J].Dis Model Mech,2013,6(6):1307-1315.
    [13]Min JW,Kong WL,Han S,et al.Vitexin protects against hypoxicischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinaseⅡand apoptosis signaling in the neonatal mouse?brain[J].Oncotarget,2017,8(15):25513-25524.
    [14]Kawabori M,Yenari MA.Inflammatory responses in brain ischemia[J].Curr Med Chem,2015,22(10):1258-1277.
    [15]Miller BA,Turan N,Chau M,et al.Inflammation,vasospasm,and brain injury after subarachnoid hemorrhage[J].Biomed Res Int,2014,2014:384342.
    [16]Li B,Concepcion K,Meng X,et al.Brain-immune interactions in perinatal hypoxic-ischemic brain injury[J].Prog Neurobiol,2017,159:50-68.
    [17]Shichita T,Ito M,Morita R,et al.MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1[J].Nat Med,2017,23(6):723-732.
    [18]Tobin MK,Bonds JA,Minshall RD,et al.Neurogenesis and inflammation after ischemic stroke:What is known and where we go from here[J].J Cereb Blood Flow Metab,2014,34(10):1573-1584.
    [19]Morioka C,Komaki M,Taki A,et al.Neuroprotective effects of human umbilical cord-derived mesenchymal stem cells on periventricular leukomalacia-like brain injury in neonatal rats[J].Inflamm Regen,2017,37:1.
    [20]Fang C,Xie L,Liu C,et al.TanshinoneⅡA improves hypoxic ischemic encephalopathy through TLR-4-mediated NF-κB signal pathway[J].Mol Med Rep,2018,18(2):1899-1908.
    [21]Seok SM,Kim JM,Park TY,et al.Fructose-1,6-bisphosphate ameliorates lipopolysaccharide-induced dysfunction of blood-brain barrier[J].Arch Pharm Res,2013,36(9):1149-1159.
    [22]Ismail R,Ul Hussain M.The up regulation of phosphofructokinase1(PFK1)protein during chemically induced hypoxia is mediated by the hypoxia-responsive internal ribosome entry site(IRES)element,present in its 5'untranslated region[J].Biochimie,2017,139:38-45.
    [23]Seok SM,Park TY,Park HS,et al.Fructose-1,6-bisphosphate suppresses lipopolysaccharide-induced expression of ICAM-1through modulation of toll-like receptor-4 signaling in brain endothelial cells[J].Int Immunopharmacol,2015,26(1):203-211.
    [24]Catarina AV,Luft C,Greggio S,et al.Fructose-1,6-bisphosphate preserves glucose metabolism integrity and reduces reactive oxygen species in the brain during experimental sepsis[J].Brain Res,2018,1698:54-61.
    [25]Park JY,Kim EJ,Kwon KJ,et al.Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK[J].Brain Res,2004,1026(2):295-301.
    [26]Kaakinen T,Heikkinen J,Dahlbacka S,et al.Fructose-1,6-bisphosphate supports cerebral energy metabolism in pigs after ischemic brain injury caused by experimental particle embolization[J].Heart Surg Forum,2006,9(6):E828-835.
    [27]Elbassuoni EA,Nazmy WH.Novel neuroprotective role of hydrogen sulfide in a rat model of stress brain injury[J].Gen Physiol Biophys,2018,37(2):233-241.
    [28]Romsi P,Kaakinen T,Kiviluoma K,et al.Fructose-1,6-bisphosphate for improved outcome after hypothermic circulatory arrest in pigs[J].J Thorac Cardiovasc Surg,2003,125(3):686-698.
    [29]刘秀琴,崔丽英,王拥军,等.1,6二磷酸果糖注射液(瑞安吉)治疗急性脑梗死的多中心、随机、双盲、安慰剂对照临床研究[J].中华老年多器官疾病杂志,2005,4(2):102-105.
    [30]Zhu XJ,Li H,Zhang C.Clinical effects of Ganglioside and fructose-1,6-diphosphate on neonatal heart and braininjuries after Asphyxia[J].Pak J Med Sci,2017,33(5):1199-1204.
    [31]Stringer JL,Xu K.Possible mechanisms for the anticonvulsant activity of fructose-1,6-diphosphate[J].Epilepsia,2008,49 Suppl 8:101-103.
    [32]Ding Y,Wang S,Zhang MM,et al.Fructose-1,6-diphosphate inhibits seizure acquisition in fast hippocampal kindling[J].Neurosci Lett,2010,477(1):33-36.
    [33]郑倩,刘红,曹弟勇,等.血红素加氧酶/一氧化碳系统在1,6-二磷酸果糖抗IL-1β致胰岛细胞凋亡中的作用[J].中国应用生理学杂志,2009,25(4):548-552.
    [34]Bi M,Li Q,Guo D,et al.Sulphoraphane improves neuronal mitochondrial function in brain tissue in acute carbon monoxide poisoning rats[J].Basic Clin Pharmacol Toxicol,2017,120(6):541-549.
    [35]Li HF,Knutson BL,Nokes SE,et al.Metabolic control of clostridium thermocellum via inhibition of hydrogenase activity and the glucose transport rate[J].Appl Microbiol Biotechnol,2012,93(4):1777-1784.
    [36]Ding Y,Wang S,Jiang Y,et al.Fructose-1,6-diphosphate protects against epileptogenesis by modifying cation-chloride co-transporters in a model of amygdaloid-kindling temporal epilepticus[J].Brain Res,2013,1539:87-94.
    [37]Shao LR,Wang G,Stafstrom CE.The glycolytic metabolite,fructose-1,6-bisphosphate,blocks epileptiform bursts by attenuating voltage-activated calcium currents in hippocampal slices[J].Front Cell Neurosci,2018,12:168.
    [38]Al-Maghrebi M,Renno WM.Altered expression profile of glycolytic enzymes during testicular ischemia reperfusion injury is associated with the p53/TIGAR pathway:Effect of fructose 1,6-diphosphate[J].Peer J,2016,4:e2195.
    [39]Zhou J,Wang F,Zhang J,et al.Repeated febrile convulsions impair hippocampal neurons and cause synaptic damage in immature rats:Neuroprotective effect of fructose-1,6-diphosphate[J].Neural Regen Res,2014,9(9):937-942.
    [40]Qi C,Zhou D,Zhu YJ,et al.Sonochemical synthesis of fructose1,6-bisphosphate dicalcium porous microspheres and their application in promotion of osteogenic differentiation[J].Mater Sci Eng C Mater Biol Appl,2017,77:846-856.
    [41]Xu K,Stringer JL.Pharmacokinetics of fructose-1,6-diphosphate after intraperitoneal and oral administration to adult rats[J].Pharmacol Res,2008,57(3):234-238.
    [42]张力,陈淑娟,杨毅梅,等.果糖二磷酸钠毒理学评价[J].同济医科大学学报,2001,30(6):530-532.
    [43]Roberts DM,Gallaptthy G,Dunuesle A,et al.Pharmcological treatment of cardiac glycoside poisoning[J].Br J Clin Pharmacol,2016,81(3):488-495.
    [44]王淑梅,张胜利.1,6二磷酸果糖药物不良反应分析[J].中国误诊学杂志,2006,6(14):2852.
    [45]宋立江,蒋东升,马晓彤,等.果糖二磷酸钠毒理学评价(二)[J].卫生毒理学杂志,2004,18(4):239-240.
    [46]吴羽琴,孙晓春,赵方园,等.注射用果糖二磷酸钠与临床常用药物的配伍禁忌[J].中外医疗,2011,30(35):100.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700