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

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 neuroscience.high-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 injury.Several 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 disorders.Although 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 disorders.In 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 role.Research 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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Role of high mobility group box protein 1 in depression:A mechanistic and therapeutic perspective

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World Journal of Psychiatry 2022年第6期12卷 779-786页

作者： Shu Wang Yu-Guang Guan Yan-Hua Zhu Min-Zhong Wang Department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China Department of Neurosurgery Sanbo Brain HospitalCapital Medical UniversityBeijing 100093China Beijing Key Laboratory of Epilepsy Center of EpilepsyBeijing Institute of Brain DisordersCollaborative Innovation Center for Brain DisordersCapital Medical UniversityBeijing 100093China Department of Cardiology Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250021Shandong ProvinceChina Department of Neurology Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250021Shandong ProvinceChina

As a common and serious psychiatric disorder,depression significantly affects psychosocial functioning and quality of life.However,the mechanism of depression is still enigmatic and perplexing,which limits its precise and effective therapeutic methods.Recent studies demonstrated that neuroinflammation activation plays an important role in the pathophysiology of depression.In this respect,high mobility group box 1(HMGB1)may be a possible signaling inducer of neuroinflammation and can be a potential mechanistic and therapeutic target for depression.Herein,we review recent studies on the mechanistic and therapeutic targets of HMGB1 in depression and propose potential perspectives on this topic.

关键词： Neuroinflammation Depression high mobility group box 1 Mechanism Review Perspective

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Changes of high mobility group box 1 in Serum of Pig Acute Hepatic Failure Model and Significance

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2008年第1期28卷 52-55页

作者：张帆贺永文段钟平 Department of Infectious Disease Union Hospital Tongji Medical Colleage Huazhong University of Science and Technology

The role of the high mobility group box 1 （HMGB-1） in acute hepatic failure and the effect of artificial liver support system treatment on HMGB-1 level were investigated. Pig models of acute hepatic failure were induced by D-galactosamine and randomly divided into two groups with or without artificial liver support system treatment. Tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） levels were detected by the enzyme linked immunosorbent assay （ELISA）, the expression of HMGB-1 by Western blot, and serum levels of HMGB-1, liver function and hepatic pathology were observed after artificial liver support system treatment. The levels of TNF-α and IL-1β were increased and reached the peak at 24th h in the acute hepatic failure group, then quickly decreased. The serum level of HMGB-1 was increased at 24th h in the acute hepatic failure group and reached the peak at 48th h, then kept a stable high level. Significant liver injury appeared at 24th h and was continuously getting worse in the pig models of acute hepatic failure. In contrast, the liver injury was significantly alleviated and serum level of HMGB-1 was significantly decreased in the group treated with artificial liver support system （P〈0.05）. It was suggested that HMGB-1 may participate in the inflammatory response and liver injury in the late stage of the acute liver failure. Artificial liver support system treatment can reduce serum HMGB-1 level and relieve liver pathological damage.

关键词： high mobility group box 1 liver failure artificial liver support system treatment

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Association between thrombomodulin and high mobility group box 1 in sepsis patients

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World Journal of Critical Care Medicine 2020年第4期9卷 63-73页

作者： Adriana Teixeira Rodrigues Julia Teixeira Rodrigues Carolina Teixeira Rodrigues Caroline Maria de Oliveira Volpe Fabiana Rocha-Silva Jose Augusto Nogueira-Machado Luiz Ronaldo Alberti Department of Pediatrics School of MedicineFederal University of Minas GeraisBelo Horizonte 30130-100Minas GeraisBrazil Graduation Program in Medicine/Biomedicine-Santa Casa Hospital-Education and Research Belo Horizonte 30150-240Minas GeraisBrazil Department of Pharmacy Federal University of Minas GeraisBelo Horizonte 31270-901Minas GeraisBrazil Department of Internal Medicine Unimed HospitalBelo Horizonte 30150-340Minas GeraisBrazil Department of Immunology Graduation Program in Medicine/Biomedicine-Santa Casa Hospital-Education and ResearchBelo Horizonte 30150-240Minas GeraisBrazil Clinical Laboratory Graduation Program in Medicine/Biomedicine-Santa Casa Hospital-Education and ResearchBelo Horizonte 30150-240Minas GeraisBrazil Department of Surgery School of MedicineFederal University of Minas GeraisBelo Horizonte 30220-000Minas GeraisBrazil

BACKGROUND high mobility group box 1(HMGB1)has been studied as a molecule associated with severe outcomes in sepsis and thrombomodulin(TM)seems to decrease HMGB1 activity.AIM To investigate the role of the thrombomodulin/high mobility group box 1(T/H)ratio in patients with sepsis and their association with their clinic,testing the hypothesis that higher ratios are associated with better outcomes.METHODS Twenty patients diagnosed with sepsis or septic shock,according to the 2016 criteria sepsis and septic shock(Sepsis-3),were studied.Patients were followed until they left the intensive care unit or until they achieved 28 d of hospitalization(D28).The following clinical outcomes were observed:Sequential Organ Failure Assessment(SOFA)score;Need for mechanical pulmonary ventilation;Presence of septic shock;Occurrence of sepsis-induced coagulopathy;Need for renal replacement therapy(RRT);and Death.RESULTS The results showed that patients with SOFA scores greater than or equal to 12 points had higher serum levels of TM:76.41±29.21 pg/mL vs 37.41±22.55 pg/mL among those whose SOFA scores were less than 12 points,P=0.003.The T/H ratio was also higher in patients whose SOFA scores were greater than or equal to 12 points,P=0.001.The T/H ratio was,on average,three times higher in patients in need of RRT(0.38±0.14 vs 0.11±0.09),P1.CONCLUSION higher serum levels of TM and,therefore,higher T/H ratio in the first 24 h after the diagnosis of sepsis were associated with more severe disease and the need for renal replacement therapy,while those with better clinical outcomes and those who were discharged before D28 showed a tendency for lower T/H ratio values.

关键词： high mobility group box 1 Sepsis Thrombomodulin Renal replacement therapy Mechanical ventilation Septic shock

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N-acetylserotonin alleviates retinal ischemia-reperfusion injury via HMGB1/RAGE/NF-κB pathway in rats

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International Journal of Ophthalmology(English edition) 2024年第2期17卷 228-238页

作者： Yu-Ze Zhao Xue-Ning Zhang Yi Yin Pei-Lun Xiao Meng Gao Lu-Ming Zhang Shuan-Hu Zhou Shu-Na Yu Xiao-Li Wang Yan-Song Zhao Department of Ophthalmology Affiliated Hospital of Weifang Medical UniversityWeifang 261031Shandong ProvinceChina School of Medical Imaging Weifang Medical UniversityWeifang 261053Shandong ProvinceChina Department of Anatomy Weifang Medical UniversityWeifang 261053Shandong ProvinceChina Departments of Orthopedic Surgery Brigham and Women’s HospitalHarvard Medical SchoolBostonMA 02115USA

AIM:To observe the effects of N-acetylserotonin(NAS)administration on retinal ischemia-reperfusion(RIR)injury in rats and explore the underlying mechanisms involving the high mobility group box 1(HMGB1)/receptor for advanced glycation end-products(RAGE)/nuclear factor-kappa B(NF-κB)signaling pathway.METHODS:A rat model of RIR was developed by increasing the pressure of the anterior chamber of the eye.Eighty male Sprague Dawley were randomly divided into five groups:sham group(n=8),RIR group(n=28),RIR+NAS group(n=28),RIR+FPS-ZM1 group(n=8)and RIR+NAS+FPS-ZM1 group(n=8).The therapeutic effects of NAS were examined by hematoxylin-eosin(H&E)staining,and retinal ganglion cells(RGCs)counting.The expression of interleukin 1 beta(IL-1β),HMGB1,RAGE,and nod-like receptor 3(NLRP3)proteins and the phosphorylation of nuclear factorkappa B(p-NF-κB)were analyzed by immunohistochemistry staining and Western blot analysis.The expression of HMGB1 protein was also detected by enzyme-linked immunosorbent assay(ELISA).RESULTS:H&E staining results showed that NAS significantly reduced retinal edema and increased the number of RGCs in RIR rats.With NAS therapy,the HMGB1 and RAGE expression decreased significantly,and the activation of the NF-κB/NLRP3 pathway was antagonized along with the inhibition of p-NF-κB and NLRP3 protein expression.Additionally,NAS exhibited an anti-inflammatory effect by reducing IL-1βexpression.The inhibitory of RAGE binding to HMGB1 by RAGE inhibitor FPS-ZM1 led to a significant decrease of p-NF-κB and NLRP3 expression,so as to the IL-1βexpression and retinal edema,accompanied by an increase of RGCs in RIR rats.CONCLUSION:NAS may exhibit a neuroprotective effect against RIR via the HMGB1/RAGE/NF-κB signaling pathway,which may be a useful therapeutic target for retinal disease.

关键词： retinal diseases retinal ischemia—reperfusion injury N-acetylserotonin high mobility group box 1 receptor for advanced glycation end-products nuclear factor-κB rats

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Celastrol mitigates inflammation in sepsis by inhibiting the PKM2-dependent Warburg effect

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Military Medical Research 2023年第1期10卷 17-31页

作者： Piao Luo Qian Zhang Tian-Yu Zhong Jia-Yun Chen Jun-Zhe Zhang Ya Tian Liu-Hai Zheng Fan Yang Ling-Yun Dai Chang Zou Zhi-Jie Li Jing-Hua Liu Ji-Gang Wang Artemisinin Research Center and Institute of Chinese Materia MedicaChinese Academy of Chinese Medical SciencesBeijing 100700China Guangdong Provincial Key Laboratory of New Drug Screening School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China Laboratory Medicine the First Affiliated Hospital of Gannan Medical UniversityGanzhou 341000JiangxiChina Department of Geriatric Medicine Shenzhen People’s Hospitalthe Second Clinical Medical CollegeJinan University and the First Affiliated HospitalSouthern University of Science and TechnologyShenzhen 518020GuangdongChina Guangdong Provincial Key Laboratory of Proteomics School of Basic Medical SciencesSouthern Medical UniversityGuangzhou 510515China Center for Reproductive Medicine Dongguan Maternal and Child Health Care HospitalSouthern Medical UniversityDongguan 523125GuangdongChina Central People’s Hospital of Zhanjiang Zhanjiang 524037GuangdongChina

Background: Sepsis involves life-threatening organ dysfunction and is caused by a dysregulated host response to infection. No specific therapies against sepsis have been reported. Celastrol(Cel) is a natural anti-inflammatory compound that shows potential against systemic inflammatory diseases. This study aimed to investigate the pharmacological activity and molecular mechanism of Cel in models of endotoxemia and sepsis.Methods: We evaluated the anti-inflammatory efficacy of Cel against endotoxemia and sepsis in mice and macrophage cultures treated with lipopolysaccharide(LPS). We screened for potential protein targets of Cel using activity-based protein profiling(ABPP). Potential targets were validated using biophysical methods such as cellular thermal shift assays(CETSA) and surface plasmon resonance(SPR). Residues involved in Cel binding to target proteins were identified through point mutagenesis, and the functional effects of such binding were explored through gene knockdown.Results: Cel protected mice from lethal endotoxemia and improved their survival with sepsis, and it significantly decreased the levels of pro-inflammatory cytokines in mice and macrophages treated with LPS(P 106 in high mobility group box 1(HMGB1) protein, reducing the secretion of inflammatory cytokine interleukin(IL)-1β. Cel bound to the Cys residues in lactate dehydrogenase A(LDHA).Conclusions: Cel inhibits inflammation and the Warburg effect in sepsis via targeting PKM2 and HMGB1 protein.

关键词： Celastrol Sepsis Pyruvate kinase M2 high mobility group box 1 Aerobic glycolysis

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Abdominal paracentesis drainage attenuates intestinal inflammation in rats with severe acute pancreatitis by inhibiting the HMGB1-mediated TLR4 signaling pathway

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World Journal of Gastroenterology 2021年第9期27卷 815-834页

作者： Shang-Qing Huang Yi Wen Hong-Yu Sun Jie Deng Yao-Lei Zhang Qi-Lin Huang Bing Wang Zhu-Lin Luo Li-Jun Tang Department of General Surgery&Pancreatic Injury and Repair Key Laboratory of Sichuan Province The General Hospital of Western Theater Command(Chengdu Military General Hospital)Chengdu 610083Sichuan ProvinceChina Basic Medical Laboratory The General Hospital of Western Theater Command(Chengdu Military General Hospital)Chengdu 610083Sichuan ProvinceChina Department of Clinical Pharmacy The General Hospital of Western Theater Command(Chengdu Military General Hospital)Chengdu 610083Sichuan ProvinceChina

BACKGROUND Our previous studies confirmed that abdominal paracentesis drainage(APD)attenuates intestinal mucosal injury in rats with severe acute pancreatitis(SAP),and improves administration of enteral nutrition in patients with acute pancreatitis(AP).However,the underlying mechanisms of the beneficial effects of APD remain poorly understood.AIM To evaluate the effect of APD on intestinal inflammation and accompanying apoptosis induced by SAP in rats,and its potential mechanisms.METHODS SAP was induced in male adult Sprague-Dawley rats by 5%sodium taurocholate.Mild AP was induced by intraperitoneal injections of cerulein(20μg/kg body weight,six consecutive injections).Following SAP induction,a drainage tube connected to a vacuum ball was placed into the lower right abdomen of the rats to build APD.Morphological changes,serum inflammatory mediators,serum and ascites high mobility group box protein 1(HMGB1),intestinal barrier function indices,apoptosis and associated proteins,and toll-like receptor 4(TLR4)signaling molecules in intestinal tissue were assessed.RESULTS APD significantly alleviated intestinal mucosal injury induced by SAP,as demonstrated by decreased pathological scores,serum levels of D-lactate,diamine oxidase and endotoxin.APD reduced intestinal inflammation and accompanying apoptosis of mucosal cells,and normalized the expression of apoptosis-associated proteins in intestinal tissues.APD significantly suppressed activation of the intestinal TLR4 signaling pathway mediated by HMGB1,thus exerting protective effects against SAP-associated intestinal injury.CONCLUSION APD improved intestinal barrier function,intestinal inflammatory response and accompanying mucosal cell apoptosis in SAP rats.The beneficial effects are potentially due to inhibition of HMGB1-mediated TLR4 signaling.

关键词： Abdominal paracentesis drainage Severe acute pancreatitis high mobility group box 1 Toll-like receptor 4 Nuclear factor-κB

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Abdominal paracentesis drainage ameliorates myocardial injury in severe experimental pancreatitis rats through suppressing oxidative stress

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World Journal of Gastroenterology 2020年第1期26卷 35-54页

作者： Yi Wen Hong-Yu Sun Zhen Tan Ruo-Hong Liu Shang-Qing Huang Guang-Yu Chen Hao Qi Li-Jun Tang Department of General Surgery and Pancreatic Injury and Repair Key Laboratory of Sichuan Province The General Hospital of Western Theater Command(Chengdu Military General Hospital)Chengdu 610083Sichuan ProvinceChina Department of Dermatology The Air Force Hospital of Western Theater CommandChengdu 610083Sichuan ProvinceChina

BACKGROUND Abdominal paracentesis drainage(APD)is a safe and effective strategy for severe acute pancreatitis(SAP)patients.However,the effects of APD treatment on SAPassociated cardiac injury remain unknown.AIM To investigate the protective effects of APD on SAP-associated cardiac injury and the underlying mechanisms.METHODS SAP was induced by 5%sodium taurocholate retrograde injection in Sprague-Dawley rats.APD was performed by inserting a drainage tube with a vacuum ball into the lower right abdomen of the rats immediately after SAP induction.Morphological staining,serum amylase and inflammatory mediators,serum and ascites high mobility group box(HMGB)1,cardiac-related enzymes indexes and cardiac function,oxidative stress markers and apoptosis and associated proteins were assessed in the myocardium in SAP rats.Nicotinamide adenine dinucleotide phosphate oxidase activity and mRNA and protein expression were also examined.RESULTS APD treatment improved cardiac morphological changes,inhibited cardiac dysfunction,decreased cardiac enzymes and reduced cardiomyocyte apoptosis,proapoptotic Bax and cleaved caspase-3 protein levels.APD significantly decreased serum levels of HMGB1,inhibited nicotinamide adenine dinucleotide phosphate oxidase expression and ultimately alleviated cardiac oxidative injury.Furthermore,the activation of cardiac nicotinamide adenine dinucleotide phosphate oxidase by pancreatitis-associated ascitic fluid intraperitoneal injection was effectively inhibited by adding anti-HMGB1 neutralizing antibody in rats with mild acute pancreatitis.CONCLUSION APD treatment could exert cardioprotective effects on SAP-associated cardiac injury through suppressing HMGB1-mediated oxidative stress,which may be a novel mechanism behind the effectiveness of APD on SAP.

关键词： Abdominal paracentesis drainage Severe acute pancreatitis Myocardial injury high mobility group box 1 Nicotinamide adenine dinucleotide phosphate oxidase Oxidative stress

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Role of immune dysfunction in drug induced liver injury

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World Journal of Hepatology 2021年第11期13卷 1677-1687页

作者： Chandrashekaran Girish Sukumaran Sanjay Department of Pharmacology Jawaharlal Institute of Postgraduate Medical Education and ResearchPuducherry 605006India

Drug-induced liver injury(DILI)is one of the leading causes of liver failure and withdrawal of drugs from the market.A poor understanding of the precipitating event aetiology and mechanisms of disease progression has rendered the prediction and subsequent treatment intractable.Recent literature suggests that some drugs can alter the liver’s repair systems resulting in injury.The pathophysiology of DILI is complex,and immune dysfunction plays an important role in determining the course and severity of the disease.Immune dysfunction is influenced by the host response to drug toxicity.A deeper understanding of these processes may be beneficial in the management of DILI and aid in drug development.This review provides a structured framework presenting DILI in three progressive stages that summarize the interplay between drugs and the host defence networks.

关键词： Immune dysfunction Liver damage Hepatotoxic drugs Drug-induced liver injury high mobility group box 1

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N-acetylcysteine and glycyrrhizin combination:Benefit outcome in a murine model of acetaminophen-induced liver failure

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World Journal of Hepatology 2020年第9期12卷 596-618页

作者： Charlotte Minsart Sandrine Rorive Arnaud Lemmers Eric Quertinmont Thierry Gustot Laboratory of Experimental Gastroenterology Erasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium Department of Pathology Erasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium DIAPATH-Center for Microscopy and Molecular Imaging UniversitéLibre de BruxellesGosselies 6041Belgium Department of Gastroenterology Hepato Pancreatology and Digestive OncologyErasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium Inserm Unité1149 Centre de Recherche sur l’inflammationParis 75006France UMR S_1149 UniversitéParis DiderotParis 75006France

BACKGROUND Acetaminophen overdose is the most frequent cause of drug-induced liver failure in developed countries.Substantial progress has been made in understanding the mechanism of hepatocellular injury,but N-acetylcysteine remains the only effective treatment despite its short therapeutic window.Thus,other hepatoprotective drugs are needed for the delayed treatment of acetaminopheninduced hepatotoxicity.Our interest focused on glycyrrhizin for its role as an inhibitor of high mobility group box 1(HMGB1)protein,a member of the family of damage-associated molecular pattern,known to play an important pathological role in various diseases.AIM To investigate the efficacy of the N-acetylcysteine/glycyrrhizin combination compared to N-acetylcysteine alone in the prevention of liver toxicity.METHODS Eight-week-old C57BL/6J wild-type female mice were used for all our experiments.Mice fasted for 15 h were treated with acetaminophen(500 mg/kg)or vehicle(phosphate-buffered saline)by intraperitoneal injection and separated into the following groups:Glycyrrhizin(200 mg/kg);N-acetylcysteine(150 mg/kg);and N-acetylcysteine/glycyrrhizin.In all groups,mice were sacrificed 12 h following acetaminophen administration.The assessment of hepatotoxicity was performed by measuring plasma levels of alanine aminotransferase,aspartate aminotransferase and lactate dehydrogenase.Hepatotoxicity was also evaluated by histological examination of hematoxylin and eosin-stained tissues sections.Survival rates were compared between various groups using Kaplan-Meier curves.RESULTS Consistent with data published in the literature,we confirmed that intraperitoneal administration of acetaminophen(500 mg/kg)in mice induced severe liver injury as evidenced by increases in alanine aminotransferase,aspartate aminotransferase and lactate dehydrogenase but also by liver necrosis score.Glycyrrhizin administration was shown to reduce the release of HMGB1 and significantly decreased the severity of liver injury.Thus,the co-administration of glycyrrhizin and N

关键词： Acetaminophen Acute liver injury Glycyrrhizin N-acetylcysteine Nacetylcysteine/glycyrrhizin combination Murine model high mobility group box 1

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