Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage

WEI Chunchun; WANG Pei; MIAO Chaoyu

doi:10.3969/j.issn.1006-0111.2016.04.003

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2016 > 34(4): 297-300,376

WEI Chunchun, WANG Pei, MIAO Chaoyu. Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 297-300,376. doi: 10.3969/j.issn.1006-0111.2016.04.003

Citation:

WEI Chunchun, WANG Pei, MIAO Chaoyu. Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 297-300,376. doi: 10.3969/j.issn.1006-0111.2016.04.003

Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage

doi: 10.3969/j.issn.1006-0111.2016.04.003

Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

Received Date: 2015-12-18
Rev Recd Date: 2016-05-04

Abstract

Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma due to the rupture of blood vessels, and is a highly lethal stroke subtype, accounting for nearly 10%-15% of all strokes. The morbidity and mortality of ICH are very high and its pathophysiological mechanisms are currently not fully understood. Therefore, based on current clinical evidence-based medicine, there is no definite and effective medical treatment that can improve the prognosis and survival of patients available yet. As an important tool for basic research, the development and application of the ICH animal model promoted the understanding of the pathophysiological mechanisms and molecular mechanisms leading to brain injury by ICH. Recently, the ICH animal model studies contributed to a number of proposed potential therapeutic strategies, such as the inhibition of thrombin and the reduction of pro-inflammatory pathways. In addition, recent research of stem cells suggested that cell transplantation therapy for the treatment of ICH may also have good prospects. In this review, we discuss the development and application of animal models for studies on ICH and the advances regarding the potential therapeutic strategies for ICH.
- intracerebral hemorrhage (ICH),
- animal model,
- neuroinflammation,
- stem cell therapy

References

[1]	Keep RF, Hua Y, Xi G. Intracerebral haemorrhage:mechanisms of injury and therapeutic targets[J]. Lancet Neurol, 2012,11(8):720-731.
[2]	Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH):a randomised trial[J]. Lancet, 2005,365(9457):387-397.
[3]	Gu Y, Hua Y, Keep RF, et al. Deferoxamine reduces intracerebral hematoma-induced iron accumulation and neuronal death in piglets[J]. Stroke, 2009,40(6):2241-2243.
[4]	Okauchi M, Hua Y, Keep RF, et al. Effects of deferoxamine on intracerebral hemorrhage-induced brain injury in aged rats[J]. Stroke, 2009,40(5):1858-1863.
[5]	Wang J, Doré S. Inflammation after intracerebral hemorrhage[J]. J Cereb Blood Flow Metab, 2007,27(5):894-908.
[6]	Wakisaka Y, Chu Y, Miller JD, et al. Spontaneous intracerebral hemorrhage during acute and chronic hypertension in mice[J]. J Cereb Blood Flow metab, 2010,30(1):56-69.
[7]	Wagner KR. Modeling intracerebral hemorrhage:glutamate, nuclear factor-kappa B signaling and cytokines[J]. Stroke, 2007,38(2 Suppl):753-758
[8]	Zhao X, Grotta J, Gonzales N, et al. Hematoma resolution as a therapeutic target:the role of microglia/macrophages[J]. Stroke, 2009,40(3 Suppl):S92-94.
[9]	Zhao X, Zhang Y, Strong R, et al. 15d-Prostaglandin J2 activates peroxisome proliferator-activated receptor-gamma, promotes expression of catalase, and reduces inflammation, behavioral dysfunction, and neuronal loss after intracerebral hemorrhage in rats[J]. J Cereb Blood Flow metab, 2006,26(6):811-820.
[10]	Zhao X, Sun G, Zhang J, et al.Hematoma resolution as a target for intracerebral hemorrhage treatment:role for peroxisome proliferator-activated receptor gamma in microglia/macrophages[J]. Ann Neurol, 2007,61(4):352-362.
[11]	Gonzales NR, Shah J, Sangha N, et al. Design of a prospective, dose-escalation study evaluating the safety of pioglitazone for hematoma resolution in intracerebral hemorrhage (SHRINC)[J]. Int J Stroke, 2013,8(5):388-396.
[12]	Zhao X, Song S, Sun G, et al. Neuroprotective role of haptoglobin after intracerebral hemorrhage[J]. J Neurosci, 2009,29(50):15819-15827.
[13]	Huang FP, Xi G, Keep RF, et al. Brain edema after experimental intracerebral hemorrhage:role of hemoglobin degradation products[J]. J Neurosurg, 2002,96(2):287-293.
[14]	Gu Y, Hua Y, He Y, et al. Iron accumulation and DNA damage in a pig model of intracerebral hemorrhage[J]. Acta Neurochir Supplement, 2011,111:123-128.
[15]	Zhou X, Xie Q, Xi G, et al. Brain CD47 expression in a swine model of intracerebral hemorrhage[J]. Brain Res, 2014,1574:70-76.
[16]	Auriat AM, Silasi G, Wei Z, et al. Ferric iron chelation lowers brain iron levels after intracerebral hemorrhage in rats but does not improve outcome[J]. Exp Neurol, 2012,234(1):136-143.
[17]	Selim M, Yeatts S, Goldstein JN, et al. Safety and tolerability of deferoxamine mesylate in patients with acute intracerebral hemorrhage[J]. Stroke, 2011,42(11):3067-3074.
[18]	Babu R, Bagley JH, Di C, et al. Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage-induced secondary brain injury and as potential targets for intervention[J]. Neurosurg Focus, 2012,32(4):E8.
[19]	Sun Z, Zhao Z, Zhao S, et al. Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo[J]. Mol Biol Rep, 2009,36(5):1119-1127.
[20]	Kitaoka T, Hua Y, Xi G, et al. Effect of delayed argatroban treatment on intracerebral hemorrhage-induced edema in the rat[J]. Acta Neurochir Suppl, 2003,86:457-461.
[21]	Xi G, Reiser G, Keep RF. The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury:deleterious or protective[J]. J Neurochem, 2003,84(1):3-9.
[22]	Hu X, Leak RK, Shi Y, et al. Microglial and macrophage polarization-new prospects for brain repair[J]. Nat Rev Neurol, 2015,11(1):56-64.
[23]	Chhor V, Le Charpentier T, Lebon S, et al. Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro[J]. Brain Behav Immun, 2013,32:70-85.
[24]	Bouhlel MA, Derudas B, Rigamonti E, et al. PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties[J]. Cell Metab, 2007,6(2):137-143.
[25]	Guo J, Chen Q, Tang J, et al. Minocycline-induced attenuation of iron overload and brain injury after experimental germinal matrix hemorrhage[J].Brain Res, 2015,1594:115-124.
[26]	Shimada K, Furukawa H, Wada KE, et al. Protective role of peroxisome proliferator-activated receptor-γ in the development of intracranial aneurysm rupture[J].Stroke, 2015,46(6):1664-1672.
[27]	Fang H, Wang PF, Zhou Y, et al. Toll-like receptor 4 signaling in intracerebral hemorrhage-induced inflammation and injury[J]. J Neuroinflamm, 2013,10:27.
[28]	Liu X, Zheng J, Zhou H. TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases[J]. Int Immunopharmacol, 2011,11(10):1451-1456.
[29]	Lin S, Yin Q, Zhong Q, et al. Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage[J]. J Neuroinflamm, 2012,9:46.
[30]	Ohnishi M, Katsuki H, Fukutomi C, et al. HMGB1 inhibitor glycyrrhizin attenuates intracerebral hemorrhage-induced injury in rats[J]. Neuropharmacology, 2011,61(5-6):975-980.
[31]	Du D, Yan J, Ren J, et al. Synthesis, biological evaluation, and molecular modeling of glycyrrhizin derivatives as potent high-mobility group box-1 inhibitors with anti-heart-failure activity in vivo[J]. J Med Chem, 2013,56(1):97-108.
[32]	Su X, Wang H, Zhao J, et al. Beneficial effects of ethyl pyruvate through inhibiting high-mobility group box 1 expression and TLR4/NF-kappaB pathway after traumatic brain injury in the rat[J]. Mediat Inflamm, 2011,2011:807142.
[33]	Lei C, Lin S, Zhang C, et al. High-mobility group box1 protein promotes neuroinflammation after intracerebral hemorrhage in rats[J]. Neuroscience, 2013,228:190-199.
[34]	Lee HJ, Kim KS, Kim EJ, et al. Brain transplantation of immortalized human neural stem cells promotes functional recovery in mouse intracerebral hemorrhage stroke model[J]. Stem Cells, 2007,25(5):1204-1212.
[35]	Bibber B, Sinha G, Lobba AR, et al. A review of stem cell translation and potential confounds by cancer stem cells[J]. Stem Cells Int, 2013,2013:241048.
[36]	Lee HK, Finniss S, Cazacu S, et al. Mesenchymal stem cells deliver exogenous miRNAs to neural cells and induce their differentiation and glutamate transporter expression[J]. Stem Cells Dev, 2014,23(23):2851-2861.
[37]	Jeon D, Chu K, Lee ST, et al. Neuroprotective effect of a cell-free extract derived from human adipose stem cells in experimental stroke models[J]. Neurobiol Dis, 2013,54:414-420.
[38]	Otero L, Zurita M, Bonilla C, et al. Allogeneic bone marrow stromal cell transplantation after cerebral hemorrhage achieves cell transdifferentiation and modulates endogenous neurogenesis[J]. Cytotherapy, 2012,14(1):34-44.

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通讯作者: 陈斌, bchen63@163.com

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沈阳化工大学材料科学与工程学院沈阳 110142

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Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage

Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

Received Date: 2015-12-18

Rev Recd Date: 2016-05-04

Key words:

Abstract: Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma due to the rupture of blood vessels, and is a highly lethal stroke subtype, accounting for nearly 10%-15% of all strokes. The morbidity and mortality of ICH are very high and its pathophysiological mechanisms are currently not fully understood. Therefore, based on current clinical evidence-based medicine, there is no definite and effective medical treatment that can improve the prognosis and survival of patients available yet. As an important tool for basic research, the development and application of the ICH animal model promoted the understanding of the pathophysiological mechanisms and molecular mechanisms leading to brain injury by ICH. Recently, the ICH animal model studies contributed to a number of proposed potential therapeutic strategies, such as the inhibition of thrombin and the reduction of pro-inflammatory pathways. In addition, recent research of stem cells suggested that cell transplantation therapy for the treatment of ICH may also have good prospects. In this review, we discuss the development and application of animal models for studies on ICH and the advances regarding the potential therapeutic strategies for ICH.

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Reference (38)

[1]	Keep RF, Hua Y, Xi G. Intracerebral haemorrhage:mechanisms of injury and therapeutic targets[J]. Lancet Neurol, 2012,11(8):720-731.
[2]	Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH):a randomised trial[J]. Lancet, 2005,365(9457):387-397.
[3]	Gu Y, Hua Y, Keep RF, et al. Deferoxamine reduces intracerebral hematoma-induced iron accumulation and neuronal death in piglets[J]. Stroke, 2009,40(6):2241-2243.
[4]	Okauchi M, Hua Y, Keep RF, et al. Effects of deferoxamine on intracerebral hemorrhage-induced brain injury in aged rats[J]. Stroke, 2009,40(5):1858-1863.
[5]	Wang J, Doré S. Inflammation after intracerebral hemorrhage[J]. J Cereb Blood Flow Metab, 2007,27(5):894-908.
[6]	Wakisaka Y, Chu Y, Miller JD, et al. Spontaneous intracerebral hemorrhage during acute and chronic hypertension in mice[J]. J Cereb Blood Flow metab, 2010,30(1):56-69.
[7]	Wagner KR. Modeling intracerebral hemorrhage:glutamate, nuclear factor-kappa B signaling and cytokines[J]. Stroke, 2007,38(2 Suppl):753-758
[8]	Zhao X, Grotta J, Gonzales N, et al. Hematoma resolution as a therapeutic target:the role of microglia/macrophages[J]. Stroke, 2009,40(3 Suppl):S92-94.
[9]	Zhao X, Zhang Y, Strong R, et al. 15d-Prostaglandin J2 activates peroxisome proliferator-activated receptor-gamma, promotes expression of catalase, and reduces inflammation, behavioral dysfunction, and neuronal loss after intracerebral hemorrhage in rats[J]. J Cereb Blood Flow metab, 2006,26(6):811-820.
[10]	Zhao X, Sun G, Zhang J, et al.Hematoma resolution as a target for intracerebral hemorrhage treatment:role for peroxisome proliferator-activated receptor gamma in microglia/macrophages[J]. Ann Neurol, 2007,61(4):352-362.
[11]	Gonzales NR, Shah J, Sangha N, et al. Design of a prospective, dose-escalation study evaluating the safety of pioglitazone for hematoma resolution in intracerebral hemorrhage (SHRINC)[J]. Int J Stroke, 2013,8(5):388-396.
[12]	Zhao X, Song S, Sun G, et al. Neuroprotective role of haptoglobin after intracerebral hemorrhage[J]. J Neurosci, 2009,29(50):15819-15827.
[13]	Huang FP, Xi G, Keep RF, et al. Brain edema after experimental intracerebral hemorrhage:role of hemoglobin degradation products[J]. J Neurosurg, 2002,96(2):287-293.
[14]	Gu Y, Hua Y, He Y, et al. Iron accumulation and DNA damage in a pig model of intracerebral hemorrhage[J]. Acta Neurochir Supplement, 2011,111:123-128.
[15]	Zhou X, Xie Q, Xi G, et al. Brain CD47 expression in a swine model of intracerebral hemorrhage[J]. Brain Res, 2014,1574:70-76.
[16]	Auriat AM, Silasi G, Wei Z, et al. Ferric iron chelation lowers brain iron levels after intracerebral hemorrhage in rats but does not improve outcome[J]. Exp Neurol, 2012,234(1):136-143.
[17]	Selim M, Yeatts S, Goldstein JN, et al. Safety and tolerability of deferoxamine mesylate in patients with acute intracerebral hemorrhage[J]. Stroke, 2011,42(11):3067-3074.
[18]	Babu R, Bagley JH, Di C, et al. Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage-induced secondary brain injury and as potential targets for intervention[J]. Neurosurg Focus, 2012,32(4):E8.
[19]	Sun Z, Zhao Z, Zhao S, et al. Recombinant hirudin treatment modulates aquaporin-4 and aquaporin-9 expression after intracerebral hemorrhage in vivo[J]. Mol Biol Rep, 2009,36(5):1119-1127.
[20]	Kitaoka T, Hua Y, Xi G, et al. Effect of delayed argatroban treatment on intracerebral hemorrhage-induced edema in the rat[J]. Acta Neurochir Suppl, 2003,86:457-461.
[21]	Xi G, Reiser G, Keep RF. The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury:deleterious or protective[J]. J Neurochem, 2003,84(1):3-9.
[22]	Hu X, Leak RK, Shi Y, et al. Microglial and macrophage polarization-new prospects for brain repair[J]. Nat Rev Neurol, 2015,11(1):56-64.
[23]	Chhor V, Le Charpentier T, Lebon S, et al. Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro[J]. Brain Behav Immun, 2013,32:70-85.
[24]	Bouhlel MA, Derudas B, Rigamonti E, et al. PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties[J]. Cell Metab, 2007,6(2):137-143.
[25]	Guo J, Chen Q, Tang J, et al. Minocycline-induced attenuation of iron overload and brain injury after experimental germinal matrix hemorrhage[J].Brain Res, 2015,1594:115-124.
[26]	Shimada K, Furukawa H, Wada KE, et al. Protective role of peroxisome proliferator-activated receptor-γ in the development of intracranial aneurysm rupture[J].Stroke, 2015,46(6):1664-1672.
[27]	Fang H, Wang PF, Zhou Y, et al. Toll-like receptor 4 signaling in intracerebral hemorrhage-induced inflammation and injury[J]. J Neuroinflamm, 2013,10:27.
[28]	Liu X, Zheng J, Zhou H. TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases[J]. Int Immunopharmacol, 2011,11(10):1451-1456.
[29]	Lin S, Yin Q, Zhong Q, et al. Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage[J]. J Neuroinflamm, 2012,9:46.
[30]	Ohnishi M, Katsuki H, Fukutomi C, et al. HMGB1 inhibitor glycyrrhizin attenuates intracerebral hemorrhage-induced injury in rats[J]. Neuropharmacology, 2011,61(5-6):975-980.
[31]	Du D, Yan J, Ren J, et al. Synthesis, biological evaluation, and molecular modeling of glycyrrhizin derivatives as potent high-mobility group box-1 inhibitors with anti-heart-failure activity in vivo[J]. J Med Chem, 2013,56(1):97-108.
[32]	Su X, Wang H, Zhao J, et al. Beneficial effects of ethyl pyruvate through inhibiting high-mobility group box 1 expression and TLR4/NF-kappaB pathway after traumatic brain injury in the rat[J]. Mediat Inflamm, 2011,2011:807142.
[33]	Lei C, Lin S, Zhang C, et al. High-mobility group box1 protein promotes neuroinflammation after intracerebral hemorrhage in rats[J]. Neuroscience, 2013,228:190-199.
[34]	Lee HJ, Kim KS, Kim EJ, et al. Brain transplantation of immortalized human neural stem cells promotes functional recovery in mouse intracerebral hemorrhage stroke model[J]. Stem Cells, 2007,25(5):1204-1212.
[35]	Bibber B, Sinha G, Lobba AR, et al. A review of stem cell translation and potential confounds by cancer stem cells[J]. Stem Cells Int, 2013,2013:241048.
[36]	Lee HK, Finniss S, Cazacu S, et al. Mesenchymal stem cells deliver exogenous miRNAs to neural cells and induce their differentiation and glutamate transporter expression[J]. Stem Cells Dev, 2014,23(23):2851-2861.
[37]	Jeon D, Chu K, Lee ST, et al. Neuroprotective effect of a cell-free extract derived from human adipose stem cells in experimental stroke models[J]. Neurobiol Dis, 2013,54:414-420.
[38]	Otero L, Zurita M, Bonilla C, et al. Allogeneic bone marrow stromal cell transplantation after cerebral hemorrhage achieves cell transdifferentiation and modulates endogenous neurogenesis[J]. Cytotherapy, 2012,14(1):34-44.

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Research progress on animal model and potential therapeutic strategy in intracerebral hemorrhage

doi: 10.3969/j.issn.1006-0111.2016.04.003

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通讯作者: 陈斌, bchen63@163.com

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