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Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

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Neural Regeneration Research 2014年第19期9卷 1731-1739页

作者： Bing Chun Yan Joon Ha Park Bai Hui Chen Jeong-hwi cho In Hye Kim Ji Hyeon Ahn Jae-Chul Lee In Koo Hwang jun hwi cho Yun Lyul Lee Il-jun Kang Moo-Ho Won Department of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Department of Anatomy and Cell Biology College of Veterinary MedicineSeoul National University Department of Emergency Medicine School of MedicineKangwon National University Department of Food Science and Nutrition Hallym University

Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperito- neal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen （NeuN; a neuronal marker） and Fluoro-]ade B （a marker for the localization of neuronal degeneration） was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67 （a marker for proliferating cells）-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin （DCX; a marker for newly generated neurons）-im- munoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2＇-deoxyuridine （BrdU）-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature BrdU/NeuN double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death.

关键词： nerve regeneration neurogenesis scopolamine dentate gyrus cell proliferation neuroblastdifferentiation neuroblast migration granule cell layer neural regeneration

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Activation of immediate-early response gene c-Fos protein in the rat paralimbic cortices after myocardial infarction

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Neural Regeneration Research 2015年第8期10卷 1251-1257页

作者： Ji Yun Ahn Hyun-Jin Tae Jeong-hwi cho In Hye Kim Ji Hyeon Ahn Joon Ha Park Dong Won Kim jun hwi cho Moo-Ho Won Seongkweon Hong Jae-Chul Lee Jeong Yeol Seo Department of Emergency Medicine Sacred Heart Hospital College of Medicine Hallym University Department of Emergency Medicine School of Medicine Kangwon National University Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Department of Neurobiology School of Medicine Kangwon National University Department of Emergency Medicine Chuncheon Sacred Heart Hospital College of Medicine Hallym University Department of Surgery School of Medicine Kangwon National University

c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.

关键词： nerve regeneration paralimbic cortices myocardial infarction c-Fos cingulate cortex piriform cortex immunohistochemistry western analysis neural regeneration

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Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia

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Neural Regeneration Research 2015年第10期10卷 1604-1611页

作者： Seongkweon Hong Ji Yun Ahn Geum-Sil cho In Hye Kim Jeong hwi cho Ji Hyeon Ahn Joon Ha Park Moo-Ho Won Bai Hui Chen Bich-Na Shin Hyun-Jin Tae Seung Min Park jun hwi cho Soo Young choi Jae-Chul Lee Department of Surgery School of Medicine Kangwon National University Department of Emergency Medicine Sacred Heart Hospital College of Medicine Hallym University Department of Emergency Medicine School of Medicine Kangwon National University Department of Neuroscience College of Medicine Korea University Department of Neurobiology School of Medicine Kangwon National University Department of Physiology College of Medicine Hallym University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University

Monocarboxylate transporters（MCTs）, which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning（IPC） on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups（sham-operated group, ischemia only group, IPC ＋ sham-operated group and IPC ＋ ischemia group）. A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region（CA1）, not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC ＋ ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC ＋ sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC ＋ ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.

关键词： nerve regeneration monocarboxylate transporters ischemic preconditioning ischemia/ reperfusion injury hippocampus CA1 pyramidal neurons neural regeneration

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Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

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Neural Regeneration Research 2017年第12期12卷 2007-2013页

作者： Hyun-Jin Tae Il jun Kang Tae-Kyeong Lee Jeong hwi cho Jae-Chul Lee Myoung Cheol Shin Yoon Sung Kim jun hwi cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah Lee Yang Hee Kim Moo-Ho Won Young Joo Lee Bio-Safety Research Institute College of Veterinary Medicine Chonbuk National University Iksan South Korea Department of Food Science and Nutrition Hallym University Chuncheon South Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Samcheok Medical Center Samcheok South Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon South Korea Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon South Korea Department of Obstetrics and Gynecology School of Medicine Kangwon National University Chuncheon South Korea Department of Surgery School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Seoul South Korea

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

关键词： nerve regeneration post-cardiac arrest syndrome normothermia neuronal damage gliosis tumor necrosis factor-alpha neural regeneration

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Pretreated quercetin protects gerbil hippocampal CA1 pyramidal neurons from transient cerebral ischemic injury by increasing the expression of antioxidant enzymes

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Neural Regeneration Research 2017年第2期12卷 220-227页

作者： Bai Hui Chen Joon Ha Park Ji Hyeon Ahn Jeong hwi cho In Hye Kim Jae Chul Lee Moo-Ho Won choong-Hyun Lee In Koo Hwang Jong-Dai Kim Il jun Kang jun hwi cho Bich Na Shin Yang Hee Kim Yun Lyul Lee Seung Min Park Department of Histology and Embryology Institute of NeuroscienceWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym UniversityChuncheonSouth Korea Department of Neurobiology School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Pharmacy College of PharmacyDankook UniversityCheonanSouth Korea Department of Anatomy and Cell Biology College of Veterinary Medicineand Research Institute for Veterinary ScienceSeoul National UniversitySeoulSouth Korea Division of Food Biotechnology School of BiotechnologyKangwon National UniversityChuncheonSouth Korea Department of Food Science and Nutrition Hallym UniversityChuncheonSouth Korea Department of Emergency Medicine School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Physiology College of Medicineand Institute of Neurodegeneration and NeuroregenerationHallym UniversityChuncheonSouth Korea Department of Surgery School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Emergency Medicine Sacred Heart HospitalCollege of MedicineHallym UniversityAnyangSouth Korea

Quercetin（QE; 3,5,7,3′,4′-pentahydroxyflavone）, a well-known flavonoid, has been shown to prevent against neurodegenerative disorders and ischemic insults. However, few studies are reported regarding the neuroprotective mechanisms of QE after ischemic insults. Therefore, in this study, we investigated the effects of QE on ischemic injury and the expression of antioxidant enzymes in the hippocampal CA1 region of gerbils subjected to 5 minutes of transient cerebral ischemia. QE was pre-treated once daily for 15 days before ischemia. Pretreatment with QE protected hippocampal CA1 pyramidal neurons from ischemic injury, which was confirmed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, pretreatment with QE significantly increased the expression levels of endogenous antioxidant enzymes Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in the hippocampal CA1 pyramidal neurons of animals with ischemic injury. These findings demonstrate that pretreated QE displayed strong neuroprotective effects against transient cerebral ischemia by increasing the expression of antioxidant enzymes.

关键词： nerve regeneration flavonoids transient cerebral ischemia Cu/Zn superoxide dismutase catalase Mn superoxide dismutase glutathione peroxidase neural regeneration

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Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus

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Neural Regeneration Research 2015年第6期10卷 944-950页

作者： Eun Joo Bae Bai Hui Chen Bing Chun Yan Bich Na Shin Jeong hwi cho In Hye Kim Ji Hyeon Ahn Jae Chul Lee Hyun-Jin Tae Seongkweon Hong Dong Won Kim jun hwi cho Yun Lyul Lee Moo-Ho Won Joon Ha Park Department of Pediatrics Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Institute of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Department of Surgery School of MedicineKangwon National University Department of Emergency Medicine Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Emergency Medicine School of MedicineKangwon National University

The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions （CA1-3） between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal CA1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group, p63 immunoreactivity was apparently changed in ischemic hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal CA1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal CA1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults.

关键词： p53 tumor suppressor gene family cerebral ischemia/reperfusion pyramidal neurons CA1 region delayed neuronal death immunohistochemistry western blotting neural regeneration

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Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

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Neural Regeneration Research 2016年第7期11卷 1081-1089页

作者： Seung Min Park Chan Woo Park Tae-Kyeong Lee Jeong hwi cho Joon Ha Park Jae-Chul Lee Bai Hui Chen Bich-Na Shin Ji Hyeon Ahn Hyun-Jin Tae Myoung Cheol Shin Taek Geun Ohk jun hwi cho Moo-Ho Won Soo Young choi In Hye Kim Department of Emergency Medicine Sacred Heart HospitalCollege of MedicineHallym University Department of Emergency Medicine School of MedicineKangwon National University Department of Neurobiology School of MedicineKangwon National University Department of Physiology College of MedicineHallym University Department of Biomedical Science Research Institute of Bioscience and BiotechnologyHallym University

Ischemic preconditioning（IPC） is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic ***,in this study,examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase（SOD） 1 and SOD2,catalase（CAT） and glutathione peroxidase（GPX） in the gerbil hippocampal CA1 region after transient forebrain *** neurons of the stratum pyramidale（SP） in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC（8.6%（ratio of remanent neurons） of the sham-operated group）;however,IPC prevented the pyramidal neurons from subsequent lethal ischemic injury（92.3%（ratio of remanent neurons） of the sham-operated group）.SOD1,SOD2,CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale（SP） of the hippocampal CA1 region,while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient ischemia without ***,their immunoreactivities in the sham-operated animals with IPC were similar to（SOD1,SOD2 and CAT） or higher（GPX） than those in the sham-operated animals without ***,their immunoreactivities in the stratum pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/*** of western blot analysis for SOD1,SOD2,CAT and GPX were similar to immunohistochemical *** conclusion,IPC maintained or increased the expression of antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia.

关键词： hippocampal operated antioxidant stratum subsequent superoxide glutathione neuronal hippocampus peroxidase

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Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia

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Neural Regeneration Research 2019年第8期14卷 1394-1403页

作者： Tae-Kyeong Lee Hyunjung Kim Minah Song Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Go Eun Yang Hyeyoung Kim Taek Geun Ohk Myoung Cheol Shin jun hwi cho Moo-Ho Won Depart merit of Neurobiology School of Medici ne Kangw on National University Chuncheon Gangwon Republic of Korea Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Chuncheon Gangwon Republic of Korea Department of Radiology Kangwon National University Hospital Chuncheon Gangxvon Republic of Korea Department of Anesthesiology and Pain Medicine Chungju Hospital Konkuk University School of Medicine Chungju Chungcheongbuk Republic of Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon Gangwon Republic of Korea

Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of transient ischemia can cause pyramidal neuronal death in the hippocampal cornu ammonis (CA) 1 field at 4 days after transient ischemia. In this study, we investigated the effects of 5-minute (mild), 15-minute (severe), and 20-minute (lethal) transient ischemia by bilateral common carotid artery occlusion (BCCAO) on behavioral change and neuronal death and gliosis (astrocytosis and microgliosis) in gerbil hippocampal subregions (CA1-3 region and dentate gyrus). We performed spontaneous motor activity test to evaluate gerbil locomotor activity, cresyl violet staining to detect cellular distribution, neuronal nuclei immunohistochemistry to detect neuronal distribution, and Fluoro-Jade B histofluorescence to evaluate neuronal death. We also conducted immunohistochemical staining for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 (Ibal) to evaluate astrocytosis and microgliosis, respectively. Animals subjected to 20-minute BCCAO died in at least 2 days. BCCAO for 15 minutes led to pyramidal cell death in hippocampal CA1-3 region 2 days later and granule cell death in hippocampal de匚tate gyrus 5 days later. Similar results were not found in animals subjected to 5-minute BCCAO. Gliosis was much more rapidly and severely progressed in animals subjected to 15-minute BCCAO than in those subjected to 5- minute BCCAO. Our results indicate that neuronal loss in the hippocampal formation following transient ischemia is significantly different according to regions and severity of transient ischemia. The experimental protocol was approved by Institutional Animal Care and Use Committee (AICUC) of Kangwon National University (approval No. KW-180124-1) on May 22, 2018.

关键词： transient global brain ischemia delayed neuronal death glial activation ischemic duration hippocampus spontaneous motor activity Mongolian gerbil histology neural regeneration

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Highly Elastic,Bioresorbable Polymeric Materials for Stretchable,Transient Electronic Systems

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Nano-Micro Letters 2024年第6期16卷 1-13页

作者： Jeong‑Woong Shin Dong‑Je Kim Tae‑Min Jang Won Bae Han Joong Hoon Lee Gwan‑Jin Ko Seung Min Yang Kaveti Rajaram Sungkeun Han Heeseok Kang jun Hyeon Lim Chan‑hwi Eom Amay J.Bandodkar Hanul Min Suk‑Won Hwang KU‑KIST Graduate School of Converging Science and Technology Korea University145 Anam‑roSeongbuk‑guSeoul 02841Republic of Korea SK Hynix 2091Gyeongchung‑daeroBubal‑eupIcheon‑siGyeonggi‑do 17336Republic of Korea Hanwha Systems Co. Ltd.188Pangyoyeok‑roBundang‑guSeongnam‑siGyeonggi‑do 13524Republic of Korea Department of Electrical and Computer Engineering North Carolina State UniversityRaleighNC 27606USA Center for Advanced Self‑Powered Systems of Integrated Sensors and Technologies(ASSIST) North Carolina State UniversityRaleighNC 27606USA Department of Integrative Energy Engineering Korea University145 Anam‑roSeongbuk‑guSeoul 02841Republic of Korea Biomaterials Research Center Korea Institute of Science and Technology(KIST)5 Hwarang‑ro 14‑gilSeongbuk‑guSeoul 02792Republic of Korea Semiconductor R&D Center Samsung Electronics Co.Ltd.Hwaseong‑siGyeonggi‑do 18448Republic of Korea Center for Advanced Biomolecular Recognition Biomedical Research DivisionKorea Institute of Science and Technology(KIST)Seoul 02792Republic of Korea

Substrates or encapsulants in soft and stretchable formats are key components for transient,bioresorbable electronic systems;however,elastomeric polymers with desired mechanical and biochemical properties are very limited compared to nontransient ***,we introduce a bioresorbable elastomer,poly(glycolide-co-ε-caprolactone)(PGCL),that contains excellent material properties including high elongation-at-break(<1300%),resilience and toughness,and tunable dissolution *** of PGCLs as polymer matrices,in combination with conducing polymers,yields stretchable,conductive composites for degradable interconnects,sensors,and actuators,which can reliably function under external *** of device components with wireless modules demonstrates elastic,transient electronic suture system with on-demand drug delivery for rapid recovery of postsurgical wounds in soft,time-dynamic tissues.

关键词： Biodegradable elastomer Conductive polymer composites Biomedical device Transient electronics

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High mobility group box 1 in the central nervous system:regeneration hidden beneath inflammation

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Neural Regeneration Research 2025年第1期20卷 107-115页

作者： Hanki Kim Bum jun Kim Seungyon Koh Hyo Jin cho Xuelian Jin Byung Gon Kim jun Young choi Department of Brain Science Ajou University School of MedicineSuwonSouth Korea Department of Biomedical Sciences Ajou University Graduate School of MedicineSuwonSouth Korea Department of Neurology Ajou University School of MedicineSuwonSouth Korea Department of Geriatrics The Affiliated Suqian First People’s Hospital of Nanjing Medical UniversitySuqianJiangsu ProvinceChina

High-mobility group box 1 was first discovered in the calf thymus as a DNA-binding nuclear protein and has been widely studied in diverse fields,including neurology and ***-mobility group box 1 in the extracellular space functions as a pro-inflammatory damage-associated molecular pattern,which has been proven to play an important role in a wide variety of central nervous system disorders such as ischemic stroke,Alzheimer’s disease,frontotemporal dementia,Parkinson’s disease,multiple sclerosis,epilepsy,and traumatic brain *** drugs that inhibit high-mobility group box 1 as a damage-associated molecular pattern,such as glycyrrhizin,ethyl pyruvate,and neutralizing anti-high-mobility group box 1 antibodies,are commonly used to target high-mobility group box 1 activity in central nervous system *** it is commonly known for its detrimental inflammatory effect,high-mobility group box 1 has also been shown to have beneficial pro-regenerative roles in central nervous system *** this narrative review,we provide a brief summary of the history of high-mobility group box 1 research and its characterization as a damage-associated molecular pattern,its downstream receptors,and intracellular signaling pathways,how high-mobility group box 1 exerts the repair-favoring roles in general and in the central nervous system,and clues on how to differentiate the pro-regenerative from the pro-inflammatory *** targeting high-mobility group box 1 in the central nervous system may benefit from differentiating between the two functions rather than overall suppression of high-mobility group box 1.

关键词： central nervous system damage-associated molecular pattern ethyl pyruvate glycyrhizzin high mobility group box 1 inflammation neural stem cells neurodevelopment oligodendrocyte progenitor cells redox status regeneration

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