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Suppressing high mobility group box-1 release alleviates morphine tolerance via the adenosine5'-monophosphate-activated protein kinase/heme oxygenase-1 pathway

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Neural Regeneration Research 2023年第9期18卷 2067-2074页

作者： Tong-Tong Lin Chun-Yi Jiang Lei Sheng Li Wan Wen Fan Jin-Can Li Xiao-Di Sun Chen-Jie Xu Liang Hu Xue-Feng Wu Yuan Han Wen-Tao Liu Yin-Bing Pan Jiangsu Key Laboratory of Neurodegeneration Department of PharmacologyNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology The First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology and Pain Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina State Key Laboratory of Pharmaceutical Biotechnology Nanjing UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology Eye&ENT HospitalFudan UniversityShanghaiChina Institute of Translational Medicine Nanjing Medical UniversityNanjingJiangsu ProvinceChina

Opioids,such as morphine,are the most potent drugs used to treat ***-term use results in high tolerance to *** mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory pain,but its role in morphine tolerance is *** this study,we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive *** found that morphine induced rat spinal cord neurons to release a large amount of ***1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4receptor expression in microglia,thereby inducing morphine ***,an HMGB1 inhibito r,markedly attenuated chronic morphine tole rance in the mouse ***,compound C(adenosine 5’-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin(heme oxygenase-1 inhibitor)alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-SY5Y cell model of morphine tole rance,and alleviated morphine tolerance in the mouse *** findings suggest that morphine induces HMGB1 release via the adenosine 5’-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway,and that inhibiting this signaling pathway can effectively reduce morphine tole rance.

关键词： adenosine 5’-monophosphate-activated protein kinase heme oxygenase-1 high mobility group box-1 interleukin-1β microglia morphine tolerance neuroinflammation neuron nuclear factor-κB p65 Toll-like receptor 4

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Predictive Value of high mobility group box-1 and miR-146b in Septic Shock Patients

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Wuhan University Journal of Natural Sciences 2024年第1期29卷 85-94页

作者： FENG Jun SHAO Shasha LIU Junya PAN Yongjun YIN Huimei WANG Junshuai Department of Emergency Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030HubeiChina Department of Critical Care Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030HubeiChina Department of Critical Care Medicine Southern University of Science and Technology HospitalShenzhen 518055GuangdongChina Department of Emergency Medicine People's Hospital of Bortala Mongol Autonomous PrefectureBole 833400XinjiangChina

In the face of the elevated incidence and mortality rate of septic shock in the ICU,this retrospective study seeks to investigate the indicative and predictive value of high-mobility group box 1(HMGB1)and miR-146b in patients with septic *** RTPCR was employed in this study to quantify the HMGB1 and miR-146b levels in plasma samples obtained from the patient group and healthy *** investigation involved the comparison between the two groups and tracking changes in the patient group over *** finding revealed that upon admission,the patient group exhibited markedly elevated relative expression levels of HMGB1,which subsequently decreased over ***,the patient group displayed significantly reduced relative expression levels of miR-146b upon admission,which subsequently increased over time compared to the control *** operating characteristic(ROC)curves showed good predictive value for HMGB1 and *** experimental results suggest that HMGB1 and miR-146b serve as valuable and convenient biomarkers for evaluating the severity of septic shock and predicting ***,it is proposed that serum miR-146b may be inducible and potentially exerts a negative regulatory effect on the expression of HMGB1.

关键词： septic shock feedback loop high mobility group box-1 miR-146b disease severity

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Interferon regulatory factor-1 mediates the release of high mobility group box-1 in endotoxemia in mice

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Chinese Medical Journal 2013年第5期126卷 918-924页

作者： PAN Pin-hua Jon Cardinal LI Mo-li HU Cheng-ping Allan Tsung Department of Pulmonary and Critical Care Medicine XiangyaHospital Central South University Changsha Hunan 410008China Department of Surgery University of Pittsburgh Pittsburgh PA15213 USA

Background The extracellular release of the danger signal high mobility group box-1 （HMGB1） has been implicated in the pathogenesis and outcomes of sepsis. Understanding the mechanisms responsible for HMGB1 release can lead to the identification of targets that may inhibit this process. The transcription factor interferon regulatory factor-1 （IRF-1） is an important mediator of innate immune responses and has been shown to participate in mortality associated with endotoxemia; however, its role in mediating the release of HMGB1 in these settings is unknown. Methods Male IRF-1 knockout （KO） and age matched C57BL/6 wild type （WT） mice were given intraperitoneal （IP） injections of lipopolysaccharide （LPS）. In some experiments, 96 hours survival rates were observed. In other experiments, mice were sacrificed 12 hours after LPS administration and sera were harvested for future analysis. In in vitro study, RAW 264.7 murine monocyte/macrophage-like cells or primary peritoneal macrophage obtained from IRF-1 KO and WT mice were cultured for LPS mediated HMGB1 release analysis. And the mechanism for HMGB1 release was analyzed by immune-precipitation. Results IRF-1 KO mice experienced less mortality, and released less systemic HMGB1 compared to their WT counterparts. Exogenous administration of recombinant HMGB1 to IRF-1 KO mice returned the mortality rate to that seen originally in IRF-1 WT mice. Using cultures of peritoneal macrophages or RAW264.7 cells, in vitro LPS stimulation induced the release of HMGB1 in an IRF-1 dependent manner. And the janus associated kinase （JAK）-IRF-1 signal pathway appeared to participate in the signaling mechanisms of LPS-induced HMGB1 release by mediating acetylation of HMGBI. Conclusion IRF-1 plays a role in LPS induced release of HMGB1 and therefore may serve as a novel target in sepsis~

关键词： interferon regulatory factor-1 endotoxin danger signaling high mobility group box-1 acetylation

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Sodium butyrate protects against toxin-induced acute liver failure in rats

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Hepatobiliary & Pancreatic Diseases International 2014年第3期13卷 309-315页

作者： Fan Yang Li-Kun Wang Xun Li Lu-Wen Wang Xiao-Qun Han Zuo-Jiong Gong Department of Infectious Diseases Renmin Hospital of Wuhan University Department of Infectious Diseases Linyi People's Hospital

BACKGROUND: Acute liver failure(ALF) is a serious clinical syndrome with high mortality. Sodium butyrate has been shown to alleviate organ injury in a wide variety of preclinical models of critical diseases. The aim of this study was to investigate the protective effect of sodium butyrate on ALF in ***: All rats were randomly divided into control,model and sodium butyrate treatment groups. Except the control group, the rats were induced ALF animal model by subcutaneous injection of human serum albumin+D- galactosamine+lipopolysaccharide. After induction of ALF,the rats in the treatment group received sodium butyrate(500mg/kg) at 12-hour or 24-hour time point. Fourty-eight hours after ALF induction, the animals were sacrificed and samples were harvested. Serum endotoxin, high mobility group box-1(HMGB1), liver function parameters, tumor necrosis factoralpha(TNF-α) and interferon-gamma(IFN-γ) were *** expression of HMGB1 and nuclear factor-kappa B(NF-κB)p65 protein in liver tissue was detected by Western blotting. The histological changes of liver and intestine were examined. The survival duration was also ***: Serum endotoxin, alanine aminotransferase, HMGB1,TNF-α and IFN-γ were significantly increased and the liver histology showed more severe histopathological injury in the model group compared with the control group(Pgroup, sodium butyrate treatment significantly improved the histopathological changes in the liver and intestine, reduced serum endotoxin and inflammatory cytokines, suppressed HMGB1 and NF-кB p65 proteins in liver tissue, and prolonged the survival duration regardless of treatment at 12 hours or 24 hours after induction of ALF(P<0.05).CONCLUSIONS: Sodium butyrate protected the liver from toxin-induced ALF in rats. The mechanisms may be due to direct hepatoprotection and decreased intestinal permeability.

关键词： acute liver failure high mobility group box-1 nuclear factor-kappa B p65 animal model sodium butyrate

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Low-intensity aerobic exercise training attenuates airway inflammation and remodeling in a rat model of steroid-resistant asthma

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Chinese Medical Journal 2014年第17期127卷 3058-3064页

作者： Qin Qingwu Chen Xi Feng Juntao Qin Ling Hu Chengping Department of Respiratory Medicine Xiangya Hospital Central South University National Clincial Research Center for Respirator3[ Disease Changsha Hunan 410008 China Bronchial Asthma Research Center of Hunan Province Changsha Hunan 410008 China

Background Aerobic exercise can improve symptoms,reduce airway inflammation,and even ameliorate airway remodeling in asthmatic animals and ***,previous studies have focused mainly on the effect of aerobic exercise on steroid-sensitive asthma （SSA）.The goals of this study were to determine the effect of low-intensity aerobic exercise training on airway hyperresponsiveness,inflammation,and remodeling in a rat model of steroid-resistant asthma （SRA） and to identify the potential mechanisms underlying these *** Endotoxin-free ovalbumin with or without lipopolysaccharide were applied to establish rat models of SRA and SSA,*** hyperresponsiveness,inflammation,remodeling,expression of interleukin （IL）-25,IL-33,thymic stromal lymphopoietin （TSLP）,high mobility group box-1 （HMGB1）,and IL-17 in bronchoalveolar lavage fluid （BALF）,and the role of dexamethasone （DXM） were compared between these two asthmatic rat *** effect of low-intensity aerobic exercise training and anti-HMGB1 treatment on airway hyperresponsiveness,inflammation,and remodeling in SRA rats also was *** SRA rats developed neutrophil-dominated airway inflammation （（29.5±4.1）％ of the total cell numbers in BALF）,whereas SSA rats developed eosinophil-dominated airway inflammation （（24.0±6.1）％ of the total cell numbers in BALF）.Compared with SSA rats,SRA rats had more severe airway hyperresponsiveness,lower levels of IL-25 （（33.6±10.3） vs.（104.8±24.9） pg/ml）,IL-33 （（87.5±25.0） vs.（226.6±40.7） pg/ml）,and TSLP （（1 933.2±899.5） vs.（7 224.0±992.1） pg/ml）,and higher levels of HMGB1 （（21.2±4.5） vs.（5.4±1.6） ng/ml） and IL-17 （（780.5±261.7） vs.（291.4±76.4） pg/ml） in BALF （all P ＜0.05）.However,there was no significant difference in goblet cell hyperplasia,subepithelial collagen thickness,and airway smooth muscle remodeling between the two *** with control SSA rats,airway hyperresponsiveness,inflammation,and remodeling in SRA rats were less sensitive t

关键词： aerobic exercise inflammation airway remodeling steroid-resistant asthma high mobility group box-1

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Ethyl pyruvate protects against experimental acute-on-chronic liver failure in rats

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World Journal of Gastroenterology 2012年第40期18卷 5709-5718页

作者： Lu-Wen Wang Li-Kun Wang Hui Chen Cheng Fan Xun Li Can-Ming He Zuo-Jiong Gong Department of Infectious Diseases Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Institute of Infectious Diseases Hubei Center for Disease Control and Prevention Wuhan 430079 Hubei Prov- ince China

AIM： To investigate the protective effects of ethyl py- ruvate （EP） on acute-on-chronic liver failure （ACLF） in rats. METHODS： An ACLF model was established in rats, and animals were randomly divided into normal, mod- el and EP treatment groups. The rats in EP treatment group received EP （40 mg/kg） at 3 h, 6 h, 12 h and 24 h after induction of ACLF. Serum endotoxin, high mobility group box-1 （HMGB1）, alanine transaminase （ALT）, tumor necrosis factor-α （TNF-α）, interferon-α （IFN-γ）, interleukin （IL）-10 and IL-18 levels, changes of liver histology and HMGB1 expressions in liver tis- sues were detected at 48 h after induction of ACLF. The effects of EP on the survival of ACLF rats were also ***： Serum levels of endotoxin （0.394 ± 0.066 EU/mL vs 0.086±0.017 EU/mL, P 〈 0.001）, HMGB1 （35.42±10,86 μg/L vs 2.14 ± 0.27 μg/L, P 〈 0.001）, ALT （8415.87 ± 3567.54 IU/L vs 38.64 ± 8.82 IU/L, P 〈 0.001）, TNF-α （190.77 ± 12.34 ng/L vs 124.40 ± 4.12 ng/L, P 〈 0.001）, IFN-γ （715.38 ± 86.03 ng/L vs 398.66 ± 32.91 ng/L, P 〈 0.001）, IL-10 （6.85 ± 0.64 ng/L vs 3.49 ± 0.24 ng/L, P 〈 0.001） and IL-18 （85.19 ±3.49 ng/L vs 55.38 ±1.25 ng/L, P 〈 0.001） were significantly increased, and liver tissues presented se- vere pathological injury in the model group compared with the normal group, Howeverr EP administration significantly improved hepatic histopathology and re- duced the serum levels of endotoxin （0.155±0.045 EU/mL vs 0.394 ± 0.066 EU/mL vs P 〈 0.001） and in- flammatory cytokines （11.13 ± 2.58 μg/L vs 35.42 ± 10.86 μg/L for HMGB1, 3512.86 ± 972.67 IU/L vs 8415.87 ± 3567.54 IU/L for ALT, 128.55 ± 5.76 ng/L vs 190.77 ± 12.34 ng/L for TNF-α 438.16 ± 38.10 ng/L vs 715.38 ± 86.03 ng/L for IFN-γ 3.55 ± 0.36 ng/L vs 6.85 ± 0.64 ng/L for IL-10, and 60.35 ± 1.63 ng/L vs 85.19 ± 3.49 ng/L for IL-18, respectively, P 〈 0.001）, and the levels of HMGB1 in liver tissues re- gardless of treatment time after induction of ACLF. EP treatment at the four time points prolonged the me- dian survi

关键词： Acute-on-chronic liver failure Ethyl pyru-vate high mobility group box-1 Inflammatory cyto-kines Histopathology Survival time

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Effect of Low Tidal Volume, Low Tidal Volume Plus Peep and Low Tidal Volume Plus Caap on Inflammatory Factors in One Lung Ventilation

Effect of Low Tidal Volume, Low Tidal Volume Plus Peep and L...

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作者： Subash Babu Lamichhane 重庆医科大学

学位级别：硕士

Introduction: A large number of studies have indentified the use of large tidal volumes as a major risk factor for the development of lung injury in mechanically ventilated patient during one lung ventilation. Therefore we have done observation of serum HMGB1, TNF-α, IL-8 concentration changes in one-lung ventilation patients by using low tidal volume, low tidal volume plus PEEP and low tidal volume plus CPAP.Methods: 60 patients of ASA I-II undergoing lobectomy with one lung ventilation were divided into four groups. The four groups are control group （group C, n=15） having tidal volume 10mL/kg, low tidal volume group （group LTV, n=15） having tidal volume 6mL/kg, low tidal volume with positive end expiratory pressure group （group LTV+PEEP, n=15） having tidal volume 6mL/kg with PEEP 5cmH20 and low tidal volume with continuous positive airway pressure group （group LTV+CPAP, n=15） having tidal volume 6mL/kg with CPAP 5cmH2O. All the patients were induced by general anesthesia and intubated with double lumen tube. After induction of anesthesia blood sample were drawn Immediate （T1）, 1 hour after one lung ventilation （T2）, 2 hours after one lung ventilation （T3）, and 24 hours after surgery （T4）. Inflammatory mediators high moblility group box -1 （HMGB1）, Tumor necrosis factor-α（TNF-α）, Interleukin8 （IL-8） and blood gas analysis was done at several time points.Results: Compared with control group, the concentration of HMGB1, TNF-α, IL-8 were no significant difference at T1 in the other groups （P>0.05）, but the HMGB1,TNF-α, IL-8 concentration were dramatically increased and showed significance at T2, T3 and T4 （Pgroup, in the LTV+ PEEP group and LTV+ CPAP group, the HMGB1,TNFα, IL-8, level were statically significant at T2, T3 and T4 （Pgroup.Conclusion: This study suggests that low tidal volume, low tidal volume + PEEP and CPAP decrease the HM

关键词： One Lung Ventilation Low Tidal Volume Continuous Positive Airway Pressure Positive End Expiratory Pressure high mobility group box-1

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