Mechanisms of damage and treatments of cerebral ischemia and reperfusion

WU Jinhua; MA Huiping; MENG Ping; JIA Zhengping

doi:10.3969/j.issn.1006-0111.2014.06.001

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2014 > 32(6): 401-404,447

WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001

Citation:

WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001

Mechanisms of damage and treatments of cerebral ischemia and reperfusion

doi: 10.3969/j.issn.1006-0111.2014.06.001

1.
Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China;School of Pharmacy, Lanzhou University, Lanzhou 730000, China
2.
Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China

Received Date: 2013-06-07
Rev Recd Date: 2013-12-20

Abstract

To summarize the advances in mechanisms of damage and treatments of cerebral ischemia and reperfusion and forecasts future research directions.The existing achievements in literatures were summarized.Cerebral ischemia and reperfusion damage were related to inflammatory response, intracellular calcium overload, free radicals injury, release of excitatory amino acids and other factors. The treatments included reducing ischemia time, blocking glutamate receptors, free radical scavenging, inhibition of apoptosis, reducing inflammation, and promoting neuronal growth, etc. Multi-target treatment would be future directions in treatment of cerebral ischemia.
- cerebral ischemia,
- reperfusion damage,
- prevention and treatment,
- mechanism of damage

References

[1]	Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage[J].Neuropharmacology, 2008, 55(3): 310-318.
[2]	Yager JY, Ashwal S. Animal models of perinatal hypoxic-ischemic brain damage[J].Pedietr Neurol,2009, 40(3): 156-167.
[3]	Huang L, Chen N, Ge M, et al. Ca²⁺ and acidosis synergistically lead to the dysfunction of cortical GABAergic neurons during ischemia[J].Bioch Biophys Res Commun, 2010, 394(3): 709-714.
[4]	Zhang YF, Fan XJ, Li X, et al. Ginsenoside Rg1 protects neurons from hypoxic-ischemic injury possibly by inhibiting Ca²⁺ influx through NMDA receptors and L-type voltage-dependent Ca²⁺ channels[J].Eur J Pharmacol, 2008, 586(1-3): 90-99.
[5]	Szydlowska K, Tymianski M. Calcium, ischemia and excitotoxicity[J].Cell Calcium, 2010, 47(2): 122-129.
[6]	Gouriou Y, Demaurex N, Bijlenga P, et al. Mitochondrial calcium handling during ischemia-induced cell death in neurons[J].Biochimie, 2011, 93(12): 2060-2067.
[7]	Richard MJ, Connell BJ, Khan BV, et al. Cellular mechanisms by which lipoic acid confers protection during the early stages of cerebral ischemia: a possible role for calcium[J].Neurosci Res, 2011, 69(4): 299-307.
[8]	Xu J, Liu ZA, Pei DS, et al. Calcium/calmodulin-dependent kinase II facilitated GluR6 subunit serine phosphorylation through GluR6-PSD95-CaMKII signaling module assembly in cerebral ischemia injury[J].Brain Res, 2010, 1366: 197-203.
[9]	Hurtado O, Moro MA, Cardenas A, et al. Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport[J].Neurobiol Dis 2005, 18(2): 336-345.
[10]	Arranz AM, Gottlieb M, Perez-Cerda F, et al. Increased expression of glutamate transporters in subcortical white matter after transient focal cerebral ischemia[J].Neurobiol Dis, 2010, 37(1): 156-165.
[11]	Wang L, Deng S, Lu Y, et al. Increased inflammation and brain injury after transient focal cerebral ischemia in activating transcription factor 3 knockout mice[J].Neuroscience, 2012, 220: 100-108.
[12]	Ye XH, Wu Y, Guo PP, et al. Lipoxin A4 analogue protects brain and reduces inflammation in a rat model of focal cerebral ischemia reperfusion[J].Brain Res, 2010, 1323: 174-183.
[13]	Webster CM, Kelly S, Koike MA, et al. Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia[J].Neurobiol Dis, 2009, 33(2): 301-312.
[14]	del Zoppo GJ. Inflammation and the neurovascular unit in the setting of focal cerebral ischemia[J].Neuroscience, 2009, 158(3): 972-982.
[15]	Kim BJ, Kim MJ, Park JM, et al. Reduced neurogenesis after suppressed inflammation by minocycline in transient cerebral ischemia in rat[J].J Neurol Sci, 2009, 279(1-2): 70-75.
[16]	Corsani L, Bizzoco E, Pedata F, et al. Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion[J].Exp Neurol, 2008, 211(2): 433-440.
[17]	Mohammadi MT, Shid-Moosavi SM, Dehghani GA. Contribution of nitric oxide synthase (NOS) in blood-brain barrier disruption during acute focal cerebral ischemia in normal rat[J].Pathophysiology, 2012, 19(1): 13-20.
[18]	Kubo K, Nakao S, Jomura S, et al. Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats[J].Brain Res, 2009, 1279: 139-146.
[19]	Nurmi A, Miettinen TK, Puolivali J, et al. Neuroprotective properties of the non-peptidyl radical scavenger IAC in rats following transient focal cerebral ischemia[J].Brain Res, 2008, 1207: 174-181.
[20]	Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia[J].Glia, 2005, 50(4): 329-339.
[21]	Rosenberg GA. Matrix metalloproteinases in neuroinflammation[J].Glia,2002, 39(3): 279-291.
[22]	Xu L, Xiong X, Ouyang Y, et al. Heat shock protein 72 (Hsp72) improves long term recovery after focal cerebral ischemia in mice[J].Neurosci Lett, 2011, 488(3): 279-282.
[23]	Qi D, Liu H, Niu J, et al. Heat shock protein 72 inhibits c-Jun N-terminal kinase 3 signaling pathway via Akt1 during cerebral ischemia[J].J Neurol Sci, 2012, 317(1-2): 123-129.
[24]	Stetler RA, Gan Y, Zhang W, et al. Heat shock proteins: cellular and molecular mechanisms in the central nervous system[J].Prog Neurobiol, 2010, 92(2): 184-211.
[25]	Barreto GE, White RE, Xu L, et al. Effects of heat shock protein 72 (Hsp72) on evolution of astrocyte activation following stroke in the mouse[J].Exp Neurol, 2012, 238(2): 284-296.
[26]	Muhammad S, Barakat W, Stoyanov S, et al. The HMGB1 receptor RAGE mediates ischemic brain damage[J].J Neurosci, 2008, 28(46): 12023-12031.
[27]	Chang WJ, Toledo-Pereyra LH. The role of HMGB1 and HSP72 in ischemia and reperfusion injury[J].J Surg Res, 2011, 166(2): 219-221.
[28]	Strbian D, Durukan A, Pitkonen M, et al. The blood-brain barrier is continuously open for several weeks following transient focal cerebral ischemia[J].Neuroscience, 2008, 153(1): 175-181.
[29]	Mohagheghi F, Bigdeli MR, Rasoulian B, et al. The neuroprotective effect of olive leaf extract is related to improved blood-brain barrier permeability and brain edema in rat with experimental focal cerebral ischemia[J].Phytomedicine, 2011, 18(2-3): 170-175.
[30]	Xiong ZG, Zhu XM, Chu XP, et al. Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels[J].Cell, 2004, 118(6): 687-698.
[31]	Pandey AK, Hazari PP, Patnaik R, et al. The role of ASIC1a in neuroprotection elicited by quercetin in focal cerebral ischemia[J].Brain Res, 2011, 1383: 289-299.
[32]	Lee BK, Lee DH, Park S, et al. Effects of KR-33028, a novel Na⁺/H⁺ exchanger-1 inhibitor, on glutamate-induced neuronal cell death and ischemia-induced cerebral infarct[J].Brain Res, 2009, 1248: 22-30.
[33]	Kim YR, Kim HN, Jang JY, et al. Electroacupuncture confers beneficial effects through ionotropic glutamate receptors involving phosphatidylinositol-3 kinase/Akt signaling pathway in focal cerebral ischemia in rats[J].Eur J Integrat Med, 2012, 4(4): e413-e420.
[34]	Im DS, Jeon JW, Lee JS, et al. Role of the NMDA receptor and iron on free radical production and brain damage following transient middle cerebral artery occlusion[J].Brain Res, 2012, 1455: 114-123.
[35]	Benakis C, Bonny C, Hirt L. JNK inhibition and inflammation after cerebral ischemia[J].Brain Behav Immun, 2010, 24(5): 800-811.
[36]	Emanueli C. Nerve growth factor promotes angiogenesis and ateriogenesis in ischemic hindlimbs[J]. Circulation, 2002, 106(17): 2257-2262.

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通讯作者: 陈斌, bchen63@163.com

1.
沈阳化工大学材料科学与工程学院沈阳 110142

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Mechanisms of damage and treatments of cerebral ischemia and reperfusion

1. Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China;School of Pharmacy, Lanzhou University, Lanzhou 730000, China

2. Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China

Received Date: 2013-06-07

Rev Recd Date: 2013-12-20

Key words:

Abstract: To summarize the advances in mechanisms of damage and treatments of cerebral ischemia and reperfusion and forecasts future research directions.The existing achievements in literatures were summarized.Cerebral ischemia and reperfusion damage were related to inflammatory response, intracellular calcium overload, free radicals injury, release of excitatory amino acids and other factors. The treatments included reducing ischemia time, blocking glutamate receptors, free radical scavenging, inhibition of apoptosis, reducing inflammation, and promoting neuronal growth, etc. Multi-target treatment would be future directions in treatment of cerebral ischemia.

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Reference (36)

[1]	Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage[J].Neuropharmacology, 2008, 55(3): 310-318.
[2]	Yager JY, Ashwal S. Animal models of perinatal hypoxic-ischemic brain damage[J].Pedietr Neurol,2009, 40(3): 156-167.
[3]	Huang L, Chen N, Ge M, et al. Ca²⁺ and acidosis synergistically lead to the dysfunction of cortical GABAergic neurons during ischemia[J].Bioch Biophys Res Commun, 2010, 394(3): 709-714.
[4]	Zhang YF, Fan XJ, Li X, et al. Ginsenoside Rg1 protects neurons from hypoxic-ischemic injury possibly by inhibiting Ca²⁺ influx through NMDA receptors and L-type voltage-dependent Ca²⁺ channels[J].Eur J Pharmacol, 2008, 586(1-3): 90-99.
[5]	Szydlowska K, Tymianski M. Calcium, ischemia and excitotoxicity[J].Cell Calcium, 2010, 47(2): 122-129.
[6]	Gouriou Y, Demaurex N, Bijlenga P, et al. Mitochondrial calcium handling during ischemia-induced cell death in neurons[J].Biochimie, 2011, 93(12): 2060-2067.
[7]	Richard MJ, Connell BJ, Khan BV, et al. Cellular mechanisms by which lipoic acid confers protection during the early stages of cerebral ischemia: a possible role for calcium[J].Neurosci Res, 2011, 69(4): 299-307.
[8]	Xu J, Liu ZA, Pei DS, et al. Calcium/calmodulin-dependent kinase II facilitated GluR6 subunit serine phosphorylation through GluR6-PSD95-CaMKII signaling module assembly in cerebral ischemia injury[J].Brain Res, 2010, 1366: 197-203.
[9]	Hurtado O, Moro MA, Cardenas A, et al. Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport[J].Neurobiol Dis 2005, 18(2): 336-345.
[10]	Arranz AM, Gottlieb M, Perez-Cerda F, et al. Increased expression of glutamate transporters in subcortical white matter after transient focal cerebral ischemia[J].Neurobiol Dis, 2010, 37(1): 156-165.
[11]	Wang L, Deng S, Lu Y, et al. Increased inflammation and brain injury after transient focal cerebral ischemia in activating transcription factor 3 knockout mice[J].Neuroscience, 2012, 220: 100-108.
[12]	Ye XH, Wu Y, Guo PP, et al. Lipoxin A4 analogue protects brain and reduces inflammation in a rat model of focal cerebral ischemia reperfusion[J].Brain Res, 2010, 1323: 174-183.
[13]	Webster CM, Kelly S, Koike MA, et al. Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia[J].Neurobiol Dis, 2009, 33(2): 301-312.
[14]	del Zoppo GJ. Inflammation and the neurovascular unit in the setting of focal cerebral ischemia[J].Neuroscience, 2009, 158(3): 972-982.
[15]	Kim BJ, Kim MJ, Park JM, et al. Reduced neurogenesis after suppressed inflammation by minocycline in transient cerebral ischemia in rat[J].J Neurol Sci, 2009, 279(1-2): 70-75.
[16]	Corsani L, Bizzoco E, Pedata F, et al. Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion[J].Exp Neurol, 2008, 211(2): 433-440.
[17]	Mohammadi MT, Shid-Moosavi SM, Dehghani GA. Contribution of nitric oxide synthase (NOS) in blood-brain barrier disruption during acute focal cerebral ischemia in normal rat[J].Pathophysiology, 2012, 19(1): 13-20.
[18]	Kubo K, Nakao S, Jomura S, et al. Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats[J].Brain Res, 2009, 1279: 139-146.
[19]	Nurmi A, Miettinen TK, Puolivali J, et al. Neuroprotective properties of the non-peptidyl radical scavenger IAC in rats following transient focal cerebral ischemia[J].Brain Res, 2008, 1207: 174-181.
[20]	Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia[J].Glia, 2005, 50(4): 329-339.
[21]	Rosenberg GA. Matrix metalloproteinases in neuroinflammation[J].Glia,2002, 39(3): 279-291.
[22]	Xu L, Xiong X, Ouyang Y, et al. Heat shock protein 72 (Hsp72) improves long term recovery after focal cerebral ischemia in mice[J].Neurosci Lett, 2011, 488(3): 279-282.
[23]	Qi D, Liu H, Niu J, et al. Heat shock protein 72 inhibits c-Jun N-terminal kinase 3 signaling pathway via Akt1 during cerebral ischemia[J].J Neurol Sci, 2012, 317(1-2): 123-129.
[24]	Stetler RA, Gan Y, Zhang W, et al. Heat shock proteins: cellular and molecular mechanisms in the central nervous system[J].Prog Neurobiol, 2010, 92(2): 184-211.
[25]	Barreto GE, White RE, Xu L, et al. Effects of heat shock protein 72 (Hsp72) on evolution of astrocyte activation following stroke in the mouse[J].Exp Neurol, 2012, 238(2): 284-296.
[26]	Muhammad S, Barakat W, Stoyanov S, et al. The HMGB1 receptor RAGE mediates ischemic brain damage[J].J Neurosci, 2008, 28(46): 12023-12031.
[27]	Chang WJ, Toledo-Pereyra LH. The role of HMGB1 and HSP72 in ischemia and reperfusion injury[J].J Surg Res, 2011, 166(2): 219-221.
[28]	Strbian D, Durukan A, Pitkonen M, et al. The blood-brain barrier is continuously open for several weeks following transient focal cerebral ischemia[J].Neuroscience, 2008, 153(1): 175-181.
[29]	Mohagheghi F, Bigdeli MR, Rasoulian B, et al. The neuroprotective effect of olive leaf extract is related to improved blood-brain barrier permeability and brain edema in rat with experimental focal cerebral ischemia[J].Phytomedicine, 2011, 18(2-3): 170-175.
[30]	Xiong ZG, Zhu XM, Chu XP, et al. Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels[J].Cell, 2004, 118(6): 687-698.
[31]	Pandey AK, Hazari PP, Patnaik R, et al. The role of ASIC1a in neuroprotection elicited by quercetin in focal cerebral ischemia[J].Brain Res, 2011, 1383: 289-299.
[32]	Lee BK, Lee DH, Park S, et al. Effects of KR-33028, a novel Na⁺/H⁺ exchanger-1 inhibitor, on glutamate-induced neuronal cell death and ischemia-induced cerebral infarct[J].Brain Res, 2009, 1248: 22-30.
[33]	Kim YR, Kim HN, Jang JY, et al. Electroacupuncture confers beneficial effects through ionotropic glutamate receptors involving phosphatidylinositol-3 kinase/Akt signaling pathway in focal cerebral ischemia in rats[J].Eur J Integrat Med, 2012, 4(4): e413-e420.
[34]	Im DS, Jeon JW, Lee JS, et al. Role of the NMDA receptor and iron on free radical production and brain damage following transient middle cerebral artery occlusion[J].Brain Res, 2012, 1455: 114-123.
[35]	Benakis C, Bonny C, Hirt L. JNK inhibition and inflammation after cerebral ischemia[J].Brain Behav Immun, 2010, 24(5): 800-811.
[36]	Emanueli C. Nerve growth factor promotes angiogenesis and ateriogenesis in ischemic hindlimbs[J]. Circulation, 2002, 106(17): 2257-2262.

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Mechanisms of damage and treatments of cerebral ischemia and reperfusion

doi: 10.3969/j.issn.1006-0111.2014.06.001

Abstract

References

Proportional views

通讯作者: 陈斌, bchen63@163.com

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