高遷移率族蛋白1在缺血性卒中急性期和癲癇急性發作中的研究進展_Journal of Epilepsy

Authors：

陶敏 ,  馬勛泰

成都醫學院第一附屬醫院神經內科（成都 610500）;

Corresponding?author：

馬勛泰, Email: maxuntai2002@126.com

Keywords：

HMGB1; 缺血性卒中; 癲癇; 缺血性卒中后癲癇

DOI：

10.7507/2096-0247.202204017

Video：

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Abstract Full text Figures/Tables Video References Cited by

高遷移率族蛋白1（High mobility group protein box 1， HMGB1）是在哺乳動物體內廣泛表達的一種非組蛋白染色體結合蛋白，在細胞外與糖基化終末產物受體（Glycosylation receptor，RAGE）、Toll 樣受體4（Toll-like receptors 4，TLR4）等相互作用，促進炎性因子分泌、神經元細胞生長發育及腫瘤細胞生長遷移等。HMGB1 在多種神經元疾病中均有影響，尤其在急性缺血性卒中及癲癇疾病過程中起重要作用，通過易位和釋放，結合下游受體、促進細胞興奮性、損壞血腦屏障等方式促進缺血性腦卒中及癲癇的發生發展，而目前尚未發現HMGB1在缺血性卒中后癲癇中所發揮的作用，因此該篇綜述通過總結歸納 HMGB1 在缺血性腦卒中和癲癇之間的研究機制，為其在缺血性卒中后癲癇發生機制的相關性等提供新的研究思路。

Citation： 陶敏, 馬勛泰. 高遷移率族蛋白1在缺血性卒中急性期和癲癇急性發作中的研究進展. Journal of Epilepsy, 2022, 8(5): 442-447. doi: 10.7507/2096-0247.202204017 Copy

1.	Lühdorf K, Jensen LK, Plesner AM. Etiology of seizures in the elderly. Epilepsia, 1986, 27(4): 458-463.
2.	Seshadri S, Wolf PA. Lifetime risk of stroke and dementia: current concepts, and estimates from the Framingham Study. Lancet Neurol, 2007, 6(12): 1106-1014.
3.	Beghi E, Carpio A, Forsgren L, et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia, 2010, 51(4): 671-675.
4.	Hesdorffer DC, Benn EK, Cascino GD, et al. Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure. Epilepsia, 2009, 50(5): 1102-1108.
5.	Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia, 2014, 55(4): 475-482.
6.	Ferlazzo E, Gasparini S, Beghi E, et al. Epilepsy in cerebrovascular diseases: review of experimental and clinical data with meta-analysis of risk factors. Epilepsia, 2016, 57(8): 1205-1214.
7.	Ma A, Al A, Ea A, et al. Incidence, predictors, and outcome of early seizures after mechanical thrombectomy. Journal of the Neurological Sciences, 2019, 396: 235-239.
8.	Galanopoulou AS, L?scher W, Lubbers L, et al. Antiepileptogenesis and disease modification: progress, challenges, and the path forward-Report of the Preclinical Working Group of the 2018 NINDS-sponsored antiepileptogenesis and disease modification workshop. Epilepsia Open, 2021, 6(2): 276-296.
9.	Stros M. HMGB proteins: interactions with DNA and chromatin. Biochim Biophys Acta, 2010, 1799(1-2): 101-113.
10.	Ulloa L, Messmer D. High-mobility group box 1 (HMGB1) protein: friend and foe. Cytokine Growth Factor Rev, 2006, 17(3): 189-201.
11.	Harris HE, Andersson U, Pisetsky DS. HMGB1: a multifunctional alarmin driving autoimmune and inflammatory disease. Nat Rev Rheumatol, 2012, 8(4): 195-202.
12.	Naglova H, Bucova M. HMGB1 and its physiological and pathological roles. Bratisl Lek Listy, 2012, 113(3): 163-171.
13.	Venereau E, De Leo F, Mezzapelle R, et al. HMGB1 as biomarker and drug target. Pharmacol Res, 2016, 111: 534-544.
14.	Maroso M, Balosso S, Ravizza T, et al. Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures. Nat. Med, 2010, 16(4): 413-419.
15.	Kim JB, Choi JS, Yu YM, et al. HMGB1, a novel cytokine-like mediator linking acute neuronal death and delayed neuroinflammation in the postischemic brain. J Neurosci, 2006, 26(24): 6413-6421.
16.	Wang J, Hu X, Xie J, et al. Beta-1-adrenergic receptors mediate Nrf2-HO-1-HMGB1 axis regulation to attenuate hypoxia/reoxygenation-induced cardiomyocytes injury in vitro. Cell Physiol Biochem, 2015, 35(2): 767-777.
17.	Fujita K, Motoki K, Tagawa K, et al. HMGB1, a pathogenic molecule that induces neurite degeneration via TLR4-MARCKS, is a potential therapeutic target for Alzheimer’s disease. Sci Rep, 2016, 6: 31895.
18.	Okuma Y, Liu K, Wake H, et al. Anti–high mobility group box-1 antibody therapy for traumatic brain injury. Yakugaku Zasshi, 2014, 134(6): 701-705.
19.	Sasaki T, Liu K, Agari T, et al. Anti-high mobility group box 1 antibody exerts neuroprotection in a rat model of Parkinson’s disease. Exp Neurol, 2016, 275(Pt 1): 220-231.
20.	Andersson ?, Covacu R, Sunnemark D, et al. Pivotal advance:HMGB1 expression in active lesions of human and experimental multiple sclerosis. Leukoc. Biol, 2008, 84: 1248-1255.
21.	Andersson U, Yang H, Harris, H. Extracellular HMGB1 as a therapeutic target in inflammatory diseases. Expert Opin Ther Targets, 2018, 22(3): 263-277.
22.	Bianchi ME, Crippa MP, Manfredi AA, et al. High-mobility group box 1 protein orchestrates responses to tissue damage via inflammation, innate and adaptive immunity and tissue repair. Immunol. Immunol Rev, 2017, 280(1): 74-82.
23.	Kim JB, Lim CM, Yu YM, et al. Induction and subcellular localization of high-mobility group box-1 (HMGB1) in the postischemic rat brain. J Neurosci Res, 2008, 86(5): 1125-1131.
24.	Liesz A, Dalpke A, Mracsko E, et al. DAMP signaling is a key pathway inducing immune modulation after brain injury. J Neurosci, 2015, 35(2): 583-598.
25.	Zhang J, Wu Y, Weng Z, et al. Glycyrrhizin protects brain against ischemia-reperfusion injury in mice through HMGB1-TLR4-IL-17A signaling pathway. Brain Res, 2014, 1582: 176-186.
26.	Zhang J, Takahashi HK, Liu K, et al. Anti-high mobility group box-1 monoclonal antibody protects the blood-brain barrier from ischemia-induced disruption in rats. Stroke, 2011, 42(5): 1420-1428.
27.	Wang J, Han D, Sun M, et al. A combination of remote ischemic perconditioning and cerebral ischemic postconditioning inhibits autophagy to attenuate plasma HMGB1 and induce neuroprotection against stroke in rat. J Mol Neurosci, 2016, 58(4): 424-431.
28.	Dai S, Zheng Y, WangY, et al. HMGB1, neuronal excitability and epilepsy. Acta Epileptologica, 2021, 3(1): 9.
29.	Iori V, Maroso M, Rizzi M, et al. Receptor for advanced glycation Endproducts is upregulated in temporal lobe epilepsy and contributes to experimental seizures. Neurobiol Dis, 2013, 58: 102-114.
30.	Zurolo E, Iyer A, Maroso M, et al. Activation of toll-like receptor, RAGE and HMGB1 signalling in malformations of cortical development. Brain, 2011, 134(Pt 4): 1015-1032.
31.	Zhang Z, Liu Q, Liu M, et al. Upregulation of HMGB1-TLR4 inflammatory pathway in focal cortical dysplasia type II. J Neuroinflammation, 2018, 15(1): 27.
32.	Han Y, Yang L, Liu X, et al. HMGB1/CXCL12-mediated immunity and Th17 cells might underlie highly suspected autoimmune epilepsy in elderly individuals. Neuropsychiatr Dis Treat, 2020, 16: 1285-1293.
33.	Ai P, Zhang X, Xie Z, et al. The HMGB1 is increased in CSF of patients with an anti-NMDAR encephalitis. Acta Neurol Scand, 2018, 137(2): 277-282.
34.	Lauren W, Karen T, Emanuele R, et al. High mobility group box 1 in the inflammatory pathogenesis of epilepsy: profiling circulating levels after experimental and clinical seizures. Lancet, 2014, 383(Suppl 1): S105-S105.
35.	Kan M, ong L, Zhang X, et al. Circulating high mobility group box-1 and toll-like receptor 4 expressions increase the risk and severity of epilepsy. Braz J Med Biol Res, 2019, 52(7): 230-235.
36.	Liu AH, Wu YT, Wang YP. MicroRNA-129-5p inhibits the development of autoimmune encephalomyelitis-related epilepsy by targeting HMGB1 through the TLR4/NF-kB signaling pathway. Brain Res Bull, 2017, 132: 139-149.
37.	Ravizza T, Terrone G, Salamone A, et al. High mobility group box 1 is a novel pathogenic factor and a mechanistic biomarker for epilepsy. Brain Behav Immun, 2018, 72: 14-21.
38.	Balosso S, Liu J, Bianchi ME, et al. Disulfide-containing high mobility group box-1 promotes N-methyl-D-aspartate receptor function and excitotoxicity by activating toll-like receptor 4-dependent signaling in hippocampal neurons. Antioxid Redox Signal, 2014, 21(12): 1726-1740.
39.	Iori V, Iyer AM, Ravizza T, et al. Blockade of the IL-1R1/TLR4 pathway mediates disease-modification therapeutic effects in a model of acquired epilepsy. Neurobiol Dis, 2017, 99: 12-23.
40.	De Simoni MG, Perego C, Ravizza T, etl. Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus. Eur J Neurosci, 2000, 12(7): 2623-2633.
41.	Boer K, Spliet WG, van Rijen PC, et al. Evidence of activated microglia in focal cortical dysplasia. J Neuroimmunol, 2006, 173(1-2): 188-195.
42.	Ravizza T, Boer K, Redeker S, et al. The IL-1beta system in epilepsy-associated malformations of cortical development. Neurobiol Dis, 2006, 24(1): 128-143.
43.	Zhao J, Zheng Y, Liu K, et al. HMGB1 is a therapeutic target and biomarker in diazepam-refractory status epilepticus with wide time window. Neurotherapeutics, 2020, 17(2): 710-721.
44.	Luo L, Jin Y, Kim ID, et al. Glycyrrhizin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus. Exp Neurobiol, 2013, 22(2): 107-115.
45.	Doria JW, Forgacs PB. Incidence, Implications, and Management of Seizures Following Ischemic and Hemorrhagic Stroke. Curr Neurol Neurosci Rep, 2019, 19(7): 37.
46.	Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol, 2000, 57(11): 1617-1622.
47.	Lambrakis CC, Lancman ME. The phenomenology of seizures and epilepsy after stroke. Epilepsy, 1998, 11: 233-40.
48.	Feyissa AM, Hasan TF, Meschia JF. Stroke-related epilepsy. European Journal of Neurology, 2019, 26(1): 18-23.
49.	Kamp MA, Dibue M, Schneider T, et al. Calcium and potassium channels in experimental subarachnoid hemorrhage and transient global ischemiav. Stroke Res Treat, 2012, 2012: 382146.
50.	Feher G, Gurdan Z, Gombos K, et al. Early seizures after ischemic stroke: focus on thrombolysis. CNS Spectr, 2020, 25(1): 101-113.
51.	Kim SY, Buckwalter M, Soreq H, et al. Blood-brain barrier dysfunction-induced inflammatory signaling in brain pathology and epileptogenesis. Epilepsia, 2012, 53(Suppl 6): 37-44.
52.	Tanaka T, Ihara M. Post-stroke epilepsy. Neurochem Int, 2017, 107: 219-228.
53.	Xie WJ, Dong M, Liu Q, et al. Early predictors and prevention for post-stroke epilepsy: changes in neurotransmitter levels. Translational Neuroscience, 2016, 7(1): 1-5.
54.	Sun DA, Sombati S, DeLorenzo R. Glutamate injury-induced epileptogenesis in hippocampal neurons: an in vitro model of stroke-induced “epilepsy”. Stroke, 2001, 32(10): 2344-2350.
55.	Klein P, Dingledine R, Aronica E, et al. Commonalities in epileptogenic processes from different acute brain insults: do they translate. Epilepsia, 2018, 59(1): 37-66.
56.	Zhou H, Wang N, Xu L, et al. The efficacy of gastrodin in combination with folate and vitamin B12 on patients with epilepsy after stroke and its effect on HMGB-1, IL-2 and IL-6 serum levels. Exp Ther Med, 2017, 14(5): 4801-4806.
57.	Tao S, Sun J, Hao F, et al. Effects of sodium valproate combined with lamotrigine on quality of life and serum inflammatory factors in patients with poststroke secondary epilepsy. Stroke Cerebrovasc Dis, 2020, 29(5): 104644.

1. Lühdorf K, Jensen LK, Plesner AM. Etiology of seizures in the elderly. Epilepsia, 1986, 27(4): 458-463.
2. Seshadri S, Wolf PA. Lifetime risk of stroke and dementia: current concepts, and estimates from the Framingham Study. Lancet Neurol, 2007, 6(12): 1106-1014.
3. Beghi E, Carpio A, Forsgren L, et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia, 2010, 51(4): 671-675.
4. Hesdorffer DC, Benn EK, Cascino GD, et al. Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure. Epilepsia, 2009, 50(5): 1102-1108.
5. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia, 2014, 55(4): 475-482.
6. Ferlazzo E, Gasparini S, Beghi E, et al. Epilepsy in cerebrovascular diseases: review of experimental and clinical data with meta-analysis of risk factors. Epilepsia, 2016, 57(8): 1205-1214.
7. Ma A, Al A, Ea A, et al. Incidence, predictors, and outcome of early seizures after mechanical thrombectomy. Journal of the Neurological Sciences, 2019, 396: 235-239.
8. Galanopoulou AS, L?scher W, Lubbers L, et al. Antiepileptogenesis and disease modification: progress, challenges, and the path forward-Report of the Preclinical Working Group of the 2018 NINDS-sponsored antiepileptogenesis and disease modification workshop. Epilepsia Open, 2021, 6(2): 276-296.
9. Stros M. HMGB proteins: interactions with DNA and chromatin. Biochim Biophys Acta, 2010, 1799(1-2): 101-113.
10. Ulloa L, Messmer D. High-mobility group box 1 (HMGB1) protein: friend and foe. Cytokine Growth Factor Rev, 2006, 17(3): 189-201.
11. Harris HE, Andersson U, Pisetsky DS. HMGB1: a multifunctional alarmin driving autoimmune and inflammatory disease. Nat Rev Rheumatol, 2012, 8(4): 195-202.
12. Naglova H, Bucova M. HMGB1 and its physiological and pathological roles. Bratisl Lek Listy, 2012, 113(3): 163-171.
13. Venereau E, De Leo F, Mezzapelle R, et al. HMGB1 as biomarker and drug target. Pharmacol Res, 2016, 111: 534-544.
14. Maroso M, Balosso S, Ravizza T, et al. Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures. Nat. Med, 2010, 16(4): 413-419.
15. Kim JB, Choi JS, Yu YM, et al. HMGB1, a novel cytokine-like mediator linking acute neuronal death and delayed neuroinflammation in the postischemic brain. J Neurosci, 2006, 26(24): 6413-6421.
16. Wang J, Hu X, Xie J, et al. Beta-1-adrenergic receptors mediate Nrf2-HO-1-HMGB1 axis regulation to attenuate hypoxia/reoxygenation-induced cardiomyocytes injury in vitro. Cell Physiol Biochem, 2015, 35(2): 767-777.
17. Fujita K, Motoki K, Tagawa K, et al. HMGB1, a pathogenic molecule that induces neurite degeneration via TLR4-MARCKS, is a potential therapeutic target for Alzheimer’s disease. Sci Rep, 2016, 6: 31895.
18. Okuma Y, Liu K, Wake H, et al. Anti–high mobility group box-1 antibody therapy for traumatic brain injury. Yakugaku Zasshi, 2014, 134(6): 701-705.
19. Sasaki T, Liu K, Agari T, et al. Anti-high mobility group box 1 antibody exerts neuroprotection in a rat model of Parkinson’s disease. Exp Neurol, 2016, 275(Pt 1): 220-231.
20. Andersson ?, Covacu R, Sunnemark D, et al. Pivotal advance:HMGB1 expression in active lesions of human and experimental multiple sclerosis. Leukoc. Biol, 2008, 84: 1248-1255.
21. Andersson U, Yang H, Harris, H. Extracellular HMGB1 as a therapeutic target in inflammatory diseases. Expert Opin Ther Targets, 2018, 22(3): 263-277.
22. Bianchi ME, Crippa MP, Manfredi AA, et al. High-mobility group box 1 protein orchestrates responses to tissue damage via inflammation, innate and adaptive immunity and tissue repair. Immunol. Immunol Rev, 2017, 280(1): 74-82.
23. Kim JB, Lim CM, Yu YM, et al. Induction and subcellular localization of high-mobility group box-1 (HMGB1) in the postischemic rat brain. J Neurosci Res, 2008, 86(5): 1125-1131.
24. Liesz A, Dalpke A, Mracsko E, et al. DAMP signaling is a key pathway inducing immune modulation after brain injury. J Neurosci, 2015, 35(2): 583-598.
25. Zhang J, Wu Y, Weng Z, et al. Glycyrrhizin protects brain against ischemia-reperfusion injury in mice through HMGB1-TLR4-IL-17A signaling pathway. Brain Res, 2014, 1582: 176-186.
26. Zhang J, Takahashi HK, Liu K, et al. Anti-high mobility group box-1 monoclonal antibody protects the blood-brain barrier from ischemia-induced disruption in rats. Stroke, 2011, 42(5): 1420-1428.
27. Wang J, Han D, Sun M, et al. A combination of remote ischemic perconditioning and cerebral ischemic postconditioning inhibits autophagy to attenuate plasma HMGB1 and induce neuroprotection against stroke in rat. J Mol Neurosci, 2016, 58(4): 424-431.
28. Dai S, Zheng Y, WangY, et al. HMGB1, neuronal excitability and epilepsy. Acta Epileptologica, 2021, 3(1): 9.
29. Iori V, Maroso M, Rizzi M, et al. Receptor for advanced glycation Endproducts is upregulated in temporal lobe epilepsy and contributes to experimental seizures. Neurobiol Dis, 2013, 58: 102-114.
30. Zurolo E, Iyer A, Maroso M, et al. Activation of toll-like receptor, RAGE and HMGB1 signalling in malformations of cortical development. Brain, 2011, 134(Pt 4): 1015-1032.
31. Zhang Z, Liu Q, Liu M, et al. Upregulation of HMGB1-TLR4 inflammatory pathway in focal cortical dysplasia type II. J Neuroinflammation, 2018, 15(1): 27.
32. Han Y, Yang L, Liu X, et al. HMGB1/CXCL12-mediated immunity and Th17 cells might underlie highly suspected autoimmune epilepsy in elderly individuals. Neuropsychiatr Dis Treat, 2020, 16: 1285-1293.
33. Ai P, Zhang X, Xie Z, et al. The HMGB1 is increased in CSF of patients with an anti-NMDAR encephalitis. Acta Neurol Scand, 2018, 137(2): 277-282.
34. Lauren W, Karen T, Emanuele R, et al. High mobility group box 1 in the inflammatory pathogenesis of epilepsy: profiling circulating levels after experimental and clinical seizures. Lancet, 2014, 383(Suppl 1): S105-S105.
35. Kan M, ong L, Zhang X, et al. Circulating high mobility group box-1 and toll-like receptor 4 expressions increase the risk and severity of epilepsy. Braz J Med Biol Res, 2019, 52(7): 230-235.
36. Liu AH, Wu YT, Wang YP. MicroRNA-129-5p inhibits the development of autoimmune encephalomyelitis-related epilepsy by targeting HMGB1 through the TLR4/NF-kB signaling pathway. Brain Res Bull, 2017, 132: 139-149.
37. Ravizza T, Terrone G, Salamone A, et al. High mobility group box 1 is a novel pathogenic factor and a mechanistic biomarker for epilepsy. Brain Behav Immun, 2018, 72: 14-21.
38. Balosso S, Liu J, Bianchi ME, et al. Disulfide-containing high mobility group box-1 promotes N-methyl-D-aspartate receptor function and excitotoxicity by activating toll-like receptor 4-dependent signaling in hippocampal neurons. Antioxid Redox Signal, 2014, 21(12): 1726-1740.
39. Iori V, Iyer AM, Ravizza T, et al. Blockade of the IL-1R1/TLR4 pathway mediates disease-modification therapeutic effects in a model of acquired epilepsy. Neurobiol Dis, 2017, 99: 12-23.
40. De Simoni MG, Perego C, Ravizza T, etl. Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus. Eur J Neurosci, 2000, 12(7): 2623-2633.
41. Boer K, Spliet WG, van Rijen PC, et al. Evidence of activated microglia in focal cortical dysplasia. J Neuroimmunol, 2006, 173(1-2): 188-195.
42. Ravizza T, Boer K, Redeker S, et al. The IL-1beta system in epilepsy-associated malformations of cortical development. Neurobiol Dis, 2006, 24(1): 128-143.
43. Zhao J, Zheng Y, Liu K, et al. HMGB1 is a therapeutic target and biomarker in diazepam-refractory status epilepticus with wide time window. Neurotherapeutics, 2020, 17(2): 710-721.
44. Luo L, Jin Y, Kim ID, et al. Glycyrrhizin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus. Exp Neurobiol, 2013, 22(2): 107-115.
45. Doria JW, Forgacs PB. Incidence, Implications, and Management of Seizures Following Ischemic and Hemorrhagic Stroke. Curr Neurol Neurosci Rep, 2019, 19(7): 37.
46. Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol, 2000, 57(11): 1617-1622.
47. Lambrakis CC, Lancman ME. The phenomenology of seizures and epilepsy after stroke. Epilepsy, 1998, 11: 233-40.
48. Feyissa AM, Hasan TF, Meschia JF. Stroke-related epilepsy. European Journal of Neurology, 2019, 26(1): 18-23.
49. Kamp MA, Dibue M, Schneider T, et al. Calcium and potassium channels in experimental subarachnoid hemorrhage and transient global ischemiav. Stroke Res Treat, 2012, 2012: 382146.
50. Feher G, Gurdan Z, Gombos K, et al. Early seizures after ischemic stroke: focus on thrombolysis. CNS Spectr, 2020, 25(1): 101-113.
51. Kim SY, Buckwalter M, Soreq H, et al. Blood-brain barrier dysfunction-induced inflammatory signaling in brain pathology and epileptogenesis. Epilepsia, 2012, 53(Suppl 6): 37-44.
52. Tanaka T, Ihara M. Post-stroke epilepsy. Neurochem Int, 2017, 107: 219-228.
53. Xie WJ, Dong M, Liu Q, et al. Early predictors and prevention for post-stroke epilepsy: changes in neurotransmitter levels. Translational Neuroscience, 2016, 7(1): 1-5.
54. Sun DA, Sombati S, DeLorenzo R. Glutamate injury-induced epileptogenesis in hippocampal neurons: an in vitro model of stroke-induced “epilepsy”. Stroke, 2001, 32(10): 2344-2350.
55. Klein P, Dingledine R, Aronica E, et al. Commonalities in epileptogenic processes from different acute brain insults: do they translate. Epilepsia, 2018, 59(1): 37-66.
56. Zhou H, Wang N, Xu L, et al. The efficacy of gastrodin in combination with folate and vitamin B12 on patients with epilepsy after stroke and its effect on HMGB-1, IL-2 and IL-6 serum levels. Exp Ther Med, 2017, 14(5): 4801-4806.
57. Tao S, Sun J, Hao F, et al. Effects of sodium valproate combined with lamotrigine on quality of life and serum inflammatory factors in patients with poststroke secondary epilepsy. Stroke Cerebrovasc Dis, 2020, 29(5): 104644.

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高遷移率族蛋白1在缺血性卒中急性期和癲癇急性發作中的研究進展

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