scholarly journals High-mobility group box 1 protein is involved in the protective effect of Saquinavir on ventilation-induced lung injury in mice

2017 ◽  
Vol 49 (10) ◽  
pp. 907-915 ◽  
Author(s):  
Xin Wang ◽  
Renlingzi Zhang ◽  
Yao Tong ◽  
Xibing Ding ◽  
Shuqing Jin ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protective Effect ◽  
High Mobility ◽  
High Mobility Group ◽  
Ventilation Induced Lung Injury

scholarly journals High-Mobility Group Box 1 (HMGB1) and Autophagy in Acute Lung Injury (ALI): A Review

2019 ◽  
Vol 25 ◽  
pp. 1828-1837 ◽  
Author(s):  
Lihua Qu ◽  
Chao Chen ◽  
YangYe Chen ◽  
Yi Li ◽  
Fang Tang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
High Mobility ◽  
High Mobility Group

scholarly journals In vitro and in vivo assessment of the protective effect of sufentanil in acute lung injury

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098635
Author(s):  
Qi Gao ◽  
Ningqing Chang ◽  
Donglian Liu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
High Mobility ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Hmgb1 Protein

Objectives To investigate the mechanisms underlying the protective effect of sufentanil against acute lung injury (ALI). Material and Methods Rats were administered lipopolysaccharide (LPS) by endotracheal instillation to establish a model of ALI. LPS was used to stimulate BEAS-2B cells. The targets and promoter activities of IκB were assessed using a luciferase reporter assay. Apoptosis of BEAS-2B cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Results Sufentanil treatment markedly reduced pathological changes in lung tissue, pulmonary edema and secretion of inflammatory factors associated with ALI in vivo and in vitro. In addition, sufentanil suppressed apoptosis induced by LPS and activated NF-κB both in vivo and in vitro. Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment. miR-129-5p targeted the 3ʹ untranslated region and its inhibition decreased promoter activities of IκB-α. miR-129-5p inhibition significantly weakened the protective effect of sufentanil on LPS-treated BEAS-2B cells. Conclusion Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IκB-α expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.

Therapeutic potential of recombinant thrombomodulin for lung injury after pneumonectomy via inhibition of high-mobility group box 1 in mice

2016 ◽  
Vol 81 (5) ◽  
pp. 868-875 ◽  
Author(s):  
Yusuke Takahashi ◽  
Noriyuki Matsutani ◽  
Hitoshi Dejima ◽  
Takashi Nakayama ◽  
Ryo Okamura ◽  
...  
Keyword(s):  
Lung Injury ◽  
Therapeutic Potential ◽  
High Mobility ◽  
High Mobility Group ◽  
Recombinant Thrombomodulin

The Effect of Experimental Diabetes on High Mobility Group Box 1 Protein Expression in Endotoxin-Induced Acute Lung Injury

2011 ◽  
Vol 168 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Satoshi Hagiwara ◽  
Hideo Iwasaka ◽  
Chihiro Shingu ◽  
Shigekiyo Matumoto ◽  
Akira Hasegawa ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protein Expression ◽  
Experimental Diabetes ◽  
High Mobility ◽  
High Mobility Group

scholarly journals Downregulation of high mobility group box 1 attenuates the severity of acute lung injury in endotoxemic mice

2015 ◽  
Vol 11 (6) ◽  
pp. 4513-4517 ◽  
Author(s):  
XIAOJUAN ZHANG ◽  
ZHENGGANG LUAN ◽  
YINGJIAN LIANG ◽  
YINA LIU ◽  
XIAOCHUN MA
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
High Mobility ◽  
High Mobility Group

α-Chemokine receptor blockade reduces high mobility group box 1 protein-induced lung inflammation and injury and improves survival in sepsis

2005 ◽  
Vol 289 (4) ◽  
pp. L583-L590 ◽  
Author(s):  
Xinchun Lin ◽  
Huan Yang ◽  
Tohru Sakuragi ◽  
Maowen Hu ◽  
Lin L. Mantell ◽  
...  
Keyword(s):  
Lung Injury ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Critical Role ◽  
High Mobility ◽  
High Mobility Group ◽  
Receptor Blockade ◽  
Inflammatory Injury ◽  
Receptor Inhibition

High mobility group box 1 (HMGB1) protein, a late mediator of lethality in sepsis, can induce acute inflammatory lung injury. Here, we identify the critical role of α-chemokine receptors in the HMGB1-induced inflammatory injury and show that α-chemokine receptor inhibition increases survival in sepsis, in a clinically relevant time frame. Intratracheal instillation of recombinant HMGB1 induces a neutrophilic leukocytosis, preceded by alveolar accumulation of the α-chemokine macrophage inflammatory protein-2 and accompanied by injury and increased inflammatory potential within the air spaces. To investigate the role of α-chemokine receptors in the injury, we instilled recombinant HMGB1 (0.5 μg) directly into the lungs and administered a subcutaneous α-chemokine receptor inhibitor, Antileukinate (200 μg). α-Chemokine receptor blockade reduced HMGB1-induced inflammatory injury (neutrophils: 2.9 ± 3.2 vs. 8.1 ± 2.4 × 104cells; total protein: 120 ± 48 vs. 311 ± 129 μg/ml; reactive nitrogen species: 2.3 ± 0.3 vs. 3.5 ± 1.3 μM; and macrophage migration inhibitory factor: 6.4 ± 4.2 vs. 37.4 ± 15.9 ng/ml) within the bronchoalveolar lavage fluid, indicating that HMGB1-induced inflammation and injury are α-chemokine mediated. Because HMGB1 can mediate late septic lethality, we administered Antileukinate to septic mice and observed increased survival (from 58% in controls to 89%) even when the inhibitor treatment was initiated 24 h after the induction of sepsis. These data demonstrate that α-chemokine receptor inhibition can reduce HMGB1-induced lung injury and lethality in established sepsis and may provide a novel treatment in this devastating disease.

High-mobility group box-1 protein induce inflammatory response after pulmonary injury

2015 ◽  
Vol 3 (3) ◽  
pp. 195-214
Author(s):  
Jingxian H Golemis ◽  
Laurie J Rudensky
Keyword(s):  
Lung Injury ◽  
Inflammatory Response ◽  
Intratracheal Instillation ◽  
High Mobility ◽  
Lavage Fluid ◽  
High Mobility Group ◽  
Saline Control ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Chromosomal Protein

High-mobility group box 1 (HMGB1), a highly conserved non-histone chromosomal protein, was found to act as a potent proinflammatory cytokine and a mediator that participated in the development of systemic inflammatory response. Forty wild type C57BL/6 male (25-30gms) mice were randomly divided into three groups: saline control group; anti-HMGB1 antibody treated group and untreated group. Each group received intratracheal instillation twice per week for 4 consecutive months. 24 hours after the last exposure, anaesthetize the mice with chloral hydrate, bronchoalveolar lavage fluid was collected for cytokines analysis were measured by enzyme linked immunosorbent assay (ELISA). The level of the HMGB1 in lung tissue was determined by real-time PCR and western blot. Lung were fixed with 4% paraformaldehyde for histopathological detection. The serum level of HMGB1 increased after lung injury [peaked 2-5 hr] after lung injury, furthermore this upregulation in HMGB1 associated with increased proinflammatory cytokines [TNF-α, IL-6, IL-1β]. The injection of anti-HMGB1 antibody suppressed inflammatory reaction and improved the survival rate compared with control mice [71.3% vs. 29.4% P=0.031]

scholarly journals The Protective Effect of Lidocaine on Septic Rats via the Inhibition of High Mobility Group Box 1 Expression and NF-κB Activation

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Huan-Liang Wang ◽  
Yan-Qiu Xing ◽  
Ying-Xue Xu ◽  
Fei Rong ◽  
Wei-Fu Lei ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cecal Ligation ◽  
High Mobility ◽  
Inhibitory Effect ◽  
High Mobility Group ◽  
Organ Injury ◽  
Hmgb1 Level ◽  
Multiple Organs ◽  
Hmgb1 Expression ◽  
Local Anesthetic Drug

Lidocaine, a common local anesthetic drug, has anti-inflammatory effects. It has demonstrated a protective effect in mice from septic peritonitis. However, it is unknown whether lidocaine has effects on high mobility group box 1 (HMGB1), a key mediator of inflammation. In this study, we investigated the effect of lidocaine treatment on serum HMGB1 level and HMGB1 expression in liver, lungs, kidneys, and ileum in septic rats induced by cecal ligation and puncture (CLP). We found that acute organ injury induced by CLP was mitigated by lidocaine treatment and organ function was significantly improved. The data also demonstrated that lidocaine treatment raised the survival of septic rats. Furthermore, lidocaine suppressed the level of serum HMGB1, the expression of HMGB1, and the activation of NF-κB p65 in liver, kidneys, lungs, and ileum. Taken together, these results suggest that lidocaine treatment exerts its protective effection on CLP-induced septic rats. The mechanism was relative to the inhibitory effect of lidocaine on the mRNA expression level of HMGB1 in multiple organs, release of HMGB1 to plasma, and activation of NF-κB.

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