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Succinylation modification:a potential therapeutic target in stroke

Neural Regeneration Research 2024年第4期19卷 781-787页

作者： Jie Lian Wenwu Liu Qin Hu Xiaohua Zhang department of Neurosurgery Ren Ji HospitalShanghai Jiao Tong University School of Medicine department of Diving and hyperbaric Medicine Naval Medical CenterNaval Medical University

Stroke is a leading cause of mortality and disability worldwide.Ischemic cell death triggered by the compromised supply of blood oxygen and glucose is one of the major pathophysiology of strokeinduced brain injury.Impaired mitochondrial energy metabolism is observed minutes after stroke and is closely associated with the progression of neuropathology.Recently,a new type of posttranslational modification,known as lysine succinylation,has been recognized to play a significant role in mitochondrial energy metabolism after ischemia.However,the role of succinylation modification in cell metabolism after stroke and its regulation are not well understood.We aimed to review the effects of succinylation on energy metabolism,reactive oxygen species generation,and neuroinflammation,as well as Sirtuin 5 mediated desuccinylation after stroke.We also highlight the potential of targeting succinylation/desuccinylation as a promising strategy for the treatment of stroke.The succinylation level is dynamically regulated by the nonenzymatic or enzymatic transfer of a succinyl group to a protein on lysine residues and the removal of succinyl catalyzed by desuccinylases.Mounting evidence has suggested that succinylation can regulate the metabolic pathway through modulating the activity or stability of metabolic enzymes.Sirtuins,especially Sirtuin 5,are characterized for their desuccinylation activity and have been recognized as a critical regulator of metabolism through desuccinylating numerous metabolic enzymes.Imbalance between succinylation and desuccinylation has been implicated in the pathophysiology of stroke.Pharmacological agents that enhance the activity of Sirtuin 5 have been employed to promote desuccinylation and improve mitochondrial metabolism,and neuroprotective effects of these agents have been observed in experimental stroke studies.However,their therapeutic efficacy in stroke patients should be validated.

关键词： mitochondria metabolism neuroprotection sirtuin 5 stroke succinylation modification

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A combined nanotherapeutic approach targeting farnesoid X receptor,ferroptosis,and fibrosis for nonalcoholic steatohepatitis treatment

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Acta Pharmaceutica Sinica B 2024年第5期14卷 2228-2246页

作者： Jiangtao Fu Pingping Zhang Zhiguo Sun Guodong Lu Qi Cao Yiting Chen Wenbin Wu Jiabao Zhang Chunlin Zhuang Chunquan Sheng Jiajun Xu Ying Lu Pei Wang The Center for Basic Research and Innovation of Medicine and Pharmacy(MOE) School of PharmacyNaval Medical UniversityShanghai 200433China National Demonstration Center for Experimental Pharmaceutical Education Naval Medical University/Second Military Medical UniversityShanghai 200433China department of Diving and hyperbaric Medicine Naval Special Medical CenterNaval Medical UniversityShanghai 200433China

Obeticholic acid(OCA),a farnesoid X receptor(FXR)agonist with favorable effects on fatty and glucose metabolism,has been considered the leading candidate drug for nonalcoholic steatohepatitis(NASH)treatment.However,its limited effectiveness in resolving liver fibrosis and lipotoxicity-induced cell death remains a major drawback.Ferroptosis,a newly recognized form of cell death characterized by uncontrolled lipid peroxidation,is involved in the progression of NASH.Nitric oxide(NO)is a versatile biological molecule that can degrade extracellular matrix.In this study,we developed a PEGylated thiolated hollow mesoporous silica nanoparticles(MSN)loaded with OCA,as well as a ferroptosis inhibitor liproxsatin-1 and a NO donor S-nitrosothiol(ONL@MSN).Biochemical analyses,histology,multiplexed flow cytometry,bulk-tissue RNA sequencing,and fecal 16S ribosomal RNA sequencing were utilized to evaluate the effects of the combined nanoparticle(ONL@MSN)in a mouse NASH model.Compared with the OCA-loaded nanoparticles(O@MSN),ONL@MSN not only protected against hepatic steatosis but also greatly ameliorated fibrosis and ferroptosis.ONL@MSN also displayed enhanced therapeutic actions on the maintenance of intrahepatic macrophages/monocytes homeostasis,inhibition of immune response/lipid peroxidation,and correction of microbiota dysbiosis.These findings present a promising synergistic nanotherapeutic strategy for the treatment of NASH by simultaneously targeting FXR,ferroptosis,and fibrosis.

关键词： Nonalcoholic steatohepatitis Nanotherapy Farnesoid X receptor Ferroptosis Fibrosis Obeticholic acid S-Nitrosothiol Liproxstatin-1

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The anti-inflammatory effects of exercise on autoimmune diseases:A 20-year systematic review

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Journal of Sport and Health Science 2024年第3期13卷 353-367,I0001页

作者： Beibei Luo Dao Xiang Xiaorong Ji Xuan Chen Rui Li Shuxin Zhang Yujun Meng David C.Nieman Peijie Chen School of Exercise and Health Shanghai University of SportShanghai 200438China Shanghai Key Laboratory of Human Performance Shanghai University of SportShanghai 200438China department of Diving and hyperbaric Medicine Naval Medical CenterShanghai 200433China National Key Laboratory of Immunity and Inflammation Naval Medical UniversityShanghai 200433China Human Performance Laboratory Appalachian State UniversityNorth Carolina Research CampusKannapolisNC 28081USA Research Institute for Doping Control Shanghai University of SportShanghai 200438China

Background:The anti-inflammatory effect of exercise may be an underlying factor in improving several autoimmune diseases.The aim of this systematic review was to examine the evidence on the role of exercise training in mitigating inflammation in adolescents and adults with autoimmune disease.Methods:PubMed,Web of Science,and Embase databases were systematically reviewed for related studies published between January 1,2003,and August 31,2023.All randomized and non-randomized controlled trials of exercise interventions with autoimmune disease study participants that evaluated inflammation-related biomarkers were included.The quality of evidence was assessed using the Tool for the assEssment of Study qualiTy and reporting in EXercise scale and Cochrane bias risk tool.Results:A total of 14,565 records were identified.After screening the titles,abstracts,and full texts,87 were eligible for the systematic review.These studies were conducted in 25 different countries and included a total of 2779 participants(patients with autoimmune disease,in exercise or control groups).Overall,the evidence suggests that inflammation-related markers such as C-reactive protein,interleukin 6,and tumor necrosis factor a were reduced by regular exercise interventions.Regular exercise interventions combined with multiple exercise modes were associated with greater benefits.Conclusion:Regular exercise training by patients with autoimmune disease exerts an anti-inflammatory influence.This systematic review provides support for the promotion and development of clinical exercise intervention programs for patients with autoimmune disease.Most patients with autoimmune disease can safely adopt moderate exercise training protocols,but changes in inflammation biomarkers will be modest at best.Acute exercise interventions are ineffective or even modestly but transiently pro-inflammatory.

关键词： Autoimmune diseases Cytokines Inflammation Physical activity Training

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The mechanism by which hyperbaric oxygen treatment alleviates spinal cord injury: genome-wide transcriptome analysis

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Neural Regeneration Research 2022年第12期17卷 2737-2742页

作者： Zhen-Cheng Sun Fang Liang Jing Yang Yong Hai Qing-Jun Su Xue-Hua Liu department of Orthopedic Surgery Beijing Chaoyang HospitalCapital Medical UniversityBeijingChina department of hyperbaric oxygen Beijing Chaoyang HospitalCapital Medical UniversityBeijingChina

Accumulating studies have demonstrated that hyperbaric oxygen(HBO)treatment alleviates spinal cord injury(SCI).However,the underlying mechanism by which HBO alleviates SCI remains to be elucidated.In this study,we performed genome-wide transcriptional profiling of the spinal cord between SCI mice and mice that received HBO treatment by high-throughput RNA sequencing at 1 week after SCI.We also compared genome-wide transcriptional profiles from SCI mice and sham-operated mice.We found 76 differentially co-expressed genes in sham-operated mice,SCI mice,and HBO-treated SCI mice.Using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis,we identified the biological characteristics of these differentially expressed genes from the perspectives of cell component,biological process,and molecular function.We also found enriched functional pathways including ferroptosis,calcium signaling pathway,serotonergic synapse,hypoxia-inducible factor-1 signaling pathway,cholinergic synapse,and neuroactive ligand-receptor interaction.We performed quantitative reverse transcription-polymerase chain reaction and validated that HBO treatment decreased the expression of Hspb1(heat shock protein beta 1),Hmox1(heme oxygenase 1),Ftl1(ferritin light polypeptide 1),Tnc(tenascin C)and Igfbp3(insulin-like growth factor binding protein 3)and increased the expression of Slc5a7(solute carrier family 5 choline transporter member 7)after SCI.These results revealed the genome-wide transcriptional profile of the injured spinal cord after HBO treatment.Our findings contribute to a better understanding of the mechanism by which HBO treats SCI and may provide new targets for SCI intervention.

关键词： Ftl1 genome-wide transcriptome Hmox1 Hspb1 hyperbaric oxygen Igfbp3 Slc5a7 spinal cord injury Tnc

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hyperbaric oxygen Treatment for Long COVID:From Molecular Mechanism to Clinical Practice

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Current Medical Science 2023年第6期43卷 1061-1065页

作者： Jian-qing PAN Zhi-min TIAN Lian-bi XUE department of hyperbaric oxygen Huazhong University of Science and Technology Union Shenzhen HospitalShenzhen518052China BGI-Shenzhen Shenzhen518083China

Long COVID symptoms typically occur within 3 months of an initial COVID-19 infection,last for more than 2 months,and cannot be explained by other diagnoses.The most common symptoms include fatigue,dyspnea,coughing,and cognitive impairment.The mechanisms of long COVID are not fully understood,but several hypotheses have been put forth.These include coagulation and fibrosis pathway activation,inflammatory and autoimmune manifestations,persistent virus presence,and Epstein-Barr virus reactivation.hyperbaric oxygen therapy(HBOT)is a therapeutic method in which a person inhales 100%oxygen under pressure greater than that of the atmosphere.HBOT has some therapeutic effects,including improvement of microcirculation,inhibition of cytokine release leading to a reduction in inflammatory responses,inhibition of autoimmune responses,and promotion of neurological repair.Several clinical trials have been carried out using HBOT to treat long COVID.The results suggest that HBOT helps to improve symptom severity,reduce symptom duration,and enhance patients’quality of life.It is believed that HBOT is an effective option for patients with long COVID,which is worth actively promoting.

关键词： long COVID post-COVID-19 condition SARS-CoV-2 hyperbaric oxygen therapy

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Reversible Posterior Leukoencephalopathy Syndrome in Children with Nephrotic Syndrome:a Case Report

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Chinese Medical Sciences Journal 2014年第1期29卷 55-57页

作者： Sheng-da Liu Qing-min Shen Chun-feng Lv department of hyperbaric oxygen Beijing Aerospace General Hospital

REVERSIBLE posterior leukoencephalopathy syndrome(RPLS)is a rare neurological syndrome charac-terized by headache,altered mental status,seizures,and visual disturbance,associated with reversible white matter changes.1 It has been commonly reported in patients with severe hypertension and pre-eclampsia.Here we report a case with nephrotic syndrome complicated by RPLS.

关键词：肾病综合征可逆性病例报告脑病小儿高血压患者肾病综合症神经系统

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Mechanism of delayed encephalopathy after acute carbon monoxide poisoning

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Neural Regeneration Research 2020年第12期15卷 2286-2295页

作者： Yan-Qing Huang Zheng-Rong Peng Fang-Ling Huang A-Li Yang department of hyperbaric oxygen Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina

Many hypotheses exist regarding the mechanism underlying delayed encephalopathy after acute carbon monoxide poisoning(DEACMP),including the inflammation and immune-mediated damage hypothesis and the cellular apoptosis and direct neuronal toxicity hypothesis;however,no existing hypothesis provides a satisfactory explanation for the complex clinical processes observed in DEACMP.Leucine-rich repeat and immunoglobulin-like domain-containing protein-1(LINGO-1)activates the Ras homolog gene family member A(Rho A)/Rho-associated coiled-coil containing protein kinase 2(ROCK2)signaling pathway,which negatively regulates oligodendrocyte myelination,axonal growth,and neuronal survival,causing myelin damage and participating in the pathophysiological processes associated with many central nervous system diseases.However,whether LINGO-1 is involved in DEACMP remains unclear.A DEACMP model was established in rats by allowing them to inhale 1000 ppm carbon monoxide gas for 40 minutes,followed by 3000 ppm carbon monoxide gas for an additional 20 minutes.The results showed that compared with control rats,DEACMP rats showed significantly increased water maze latency and increased protein and m RNA expression levels of LINGO-1,Rho A,and ROCK2 in the brain.Compared with normal rats,significant increases in injured neurons in the hippocampus and myelin sheath damage in the lateral geniculate body were observed in DEACMP rats.From days 1 to 21 after DEACMP,the intraperitoneal injection of retinoic acid(10 mg/kg),which can inhibit LINGO-1 expression,was able to improve the above changes observed in the DEACMP model.Therefore,the overexpression of LINGO-1 appeared to increase following carbon monoxide poisoning,activating the Rho A/ROCK2 signaling pathway,which may be an important pathophysiological mechanism underlying DEACMP.This study was reviewed and approved by the Medical Ethics Committee of Xiangya Hospital of Central South Hospital(approval No.201612684)on December 26,2016.

关键词： brain injury cell death central nervous system factor injury model pathways rat

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Acute flaccid paralysis and neurogenic respiratory failure associated with enterovirus D68 infection in children: Report of two cases

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World Journal of Clinical Cases 2021年第14期9卷 3327-3333页

作者： Yv Zhang Sheng-Yuan Wang Da-Zhi Guo Shu-Yi Pan Yan Lv department of hyperbaric oxygen The Sixth Medical Center of PLA General HospitalBeijing 100048China

BACKGROUND Acute flaccid paralysis(AFP)and neurogenic respiratory failure rarely occur in children.At the end of 2018,some children with such symptoms were admitted to our hospital.In this study,we aimed to assess two children with AFP and neurogenic respiratory failure associated with enterovirus D68(EV-D68).CASE SUMMARY Two children admitted to our hospital presented with symptoms and imaging results different from those of acute disseminated encephalomyelitis and hand,foot,and mouth disease.Their main symptoms were AFP and neurogenic respiratory failure.Magnetic resonance imaging showed severe inflammatory injury mainly to the anterior horn cells of the spinal cord.Blood and cerebrospinal fluid samples were collected to assess for pathogens,including bacteria,tuberculosis,cryptococcus,herpes virus,and coxsackie virus,and the results were negative.At the beginning,the two cases were not assessed for EV-D68 in the nasopharyngeal,blood,and cerebrospinal fluid specimens.About 2 mo later,EVD68 was detected in the stool sample of one of the cases.The symptom of AFP was caused by injury to the anterior horn cells at levels C5-L5 of the spinal cord,while neurogenic respiratory failure was at levels C3-C5.CONCLUSION We should pay attention to the detection and diagnosis of EV-D68 and make efforts to develop antivirus drugs and vaccines.

关键词： Infection Enterovirus D68 Flaccid Paralysis Neurogenic Respiratory failure Case report

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hyperbaric oxygen improves functional recovery of rats after spinal cord injury via activating stromal cell-derived factor-1/CXC chemokine receptor 4 axis and promoting brain-derived neurothrophic factor expression

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Chinese Medical Journal 2019年第6期132卷 699-706页

作者： Xiang-Long Meng Yong Hai Xi-Nuo Zhang Yun-Sheng Wang Xue-Hua Liu Lin-Lin Ma Rong Yue Gang Xu Zhuo Li Orthopedic department Beijing Chaoyang Hospital Capital Medical University Beijing 100020 China hyperbaric oxygen department Beijing Chaoyang Hospital Capital Medical University Beijing 100020 China hyperbaric oxygen department Xinjiang Uygur Autonomous Region People's Hospital Urumqi Xinjiang 830001 China

Background: Spinal cord injury (SCI) is a worldwide medical concern. This study aimed to elucidate the mechanism underlying protective effect of hyperbaric oxygen (HBO) against SCI-induced neurologic defects in rats via exploring the stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) axis and expression of brain-derived neurotrophic factor (BDNF). Methods: An acute SCI rat model was established in Sprague-Dawley rats using the Allen method. Sixty rats were divided into four groups (w = 15 in each group): sham-operated, SCI, SCI treated with HBO (SCI + HBO), and SCI treated with both HBO and AMD3100 (an antagonist of CXCR4;SCI + HBO + AMD) groups. The rats were treated with HBO twice a day for 3 days and thereafter once a day after the surgery for up to 28 days. Following the surgery, neurologic assessments were performed with the Basso-Bettie-Bresnahan (BBB) scoring system on postoperative day (POD) 7, 14, 21, and 28. Spinal cord tissues were harvested to assess the expression of SDF-1, CXCR4, and BDNF at mRNA and protein levels, using quantitative real-time polymerase chain reaction, Western blot analysis, and histopathologic analysis. Results: HBO treatment recovered SCI-induced descent of BBB scores on POD 14,(1.25±0.75 vs. 1.03 ±0.66, P< 0.05), 21 (5.27± 0.89 vs. 2.56± 1.24, P< 0.05), and 28 (11.35±0.56 vs. 4.23± 1.20, P<0.05) compared with the SCI group. Significant differences were found in the mRNA levels of SDF-1 (mRNA: day 21, SCI + HBO vs. SCI + HBO + AMD, 2.89± 1.60 vs. 1.56±0.98, P<0.05), CXCR4 (mRNA: day 7, SCI + HBO vs. SCI, 2.99± 1.60 vs. 1.31 ±0.98, P<0.05;day 14, SCI + HBO vs. SCI + HBO + AMD, 4.18± 1.60 vs. 0.80±0.34, P<0.05;day 21, SCI + HBO vs. SCI, 2.10±1.01 vs.1.15±0.03, P<0.05), and BDNF (mRNA: day 7, SCI + HBO vs. SCI, 3.04±0.41 vs. 2.75±0.31, P<0.05;day 14, SCI + HBO vs. SCI, 3.88± 1.59 vs. 1.11 ±0.40, P<0.05), indicating the involvement of SDF-1/CXCR4 axis in the protective effect of HBO. Conclusions: HBO might promote the recovery of neurologic function after SCI in

关键词： Brain-derived neurotrophic factor CXC chemokine receptor 4 hyperbaric oxygen Neurotrophic Stromal cell-derived factor-1 Spinal cord injury

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hyperbaric oxygen Treatment Improves Hearing Level via Attenuating TLR4/NF-κB Mediated Inflammation in Sudden Sensorineural Hearing Loss Patients

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Biomedical and Environmental Sciences 2020年第5期33卷 331-337页

作者： LIU Xue Hua LIANG Fang JIA Xing Yuan ZHAO Lin ZHOU Yan YANG Jing department of hyperbaric oxygen Medicine Beijing Chaoyang HospitalCapital Medical UniversityBeijing 100020China Institute of Basic Medicine Sciences Beijing Chaoyang HospitalCapital Medical UniversityBeijing 100020China department of hyperbaric oxygen Medicine Beijing Pinggu HospitalBeijing 101200China

Objective hyperbaric oxygen treatment(HBOT)has demonstrated efficacy in improving hearing levels of patients with idiopathic sudden sensorineural hearing loss(ISSHL);however,the underlying mechanisms are not well understood.HBOT alleviates the inflammatory response,which is mediated by Toll-like receptor(TLR)4 and nuclear factor(NF)-κB.In this study we investigated whether HBOT attenuates inflammation in ISHHL patients via alteration of TLR4 and NF-κB expression.Methods ISHHL patients(n=120)and healthy control subjects(n=20)were enrolled in this study.Patients were randomly divided into medicine group treated with medicine only(n=60)and HBO group receiving both HBOT and medicine(n=60).Audiometric testing was performed pre-and posttreatment.TLR4,NF-кB,and TNF-αexpression in peripheral blood of ISSHL patients and healthy control subjects was assessed by ELISA before and after treatment.Results TLR4,NF-κB,and TNF-αlevels were upregulated in ISSHL patients relative to healthy control subjects;the levels were decreased following treatment and were lower in the HBO group than that in the medicine group post-treatment(P<0.05 and P<0.01).Conclusion HBOT alleviates hearing loss in ISSHL patients by suppressing the inflammatory response induced by TLR4 and NF-κB signaling.

关键词： hyperbaric oxygen treatment Sudden sensorineural hearing loss Toll-like receptor 4 Nuclear factor-kB

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