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

10.1155/2013/570370 â—½  
2013 â—½  
Vol 2013 â—½  
pp. 1-9 â—½  
Author(s):  
Huan-Liang Wang â—½  
Yan-Qiu Xing â—½  
Ying-Xue Xu â—½  
Fei Rong â—½  
Wei-Fu Lei â—½  
...  
Keyword(s):  
Protective Effect â—½  
Cecal Ligation â—½  
High Mobility â—½  
Inhibitory Effect â—½  
High Mobility Group â—½  
Organ Injury â—½  
Hmgb1 Level â—½  
Multiple Organs â—½  
Hmgb1 Expression â—½  
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.

scholarly journals Inhibition of Cerebral High-Mobility Group Box 1 Protein Attenuates Multiple Organ Damage and Improves T Cell-Mediated Immunity in Septic Rats

2019 â—½  
Vol 2019 â—½  
pp. 1-10 â—½  
Author(s):  
Chao Ren â—½  
Xiu-hua Li â—½  
Yao Wu â—½  
Ning Dong â—½  
Ya-lin Tong â—½  
...  
Keyword(s):  
Cecal Ligation â—½  
High Mobility â—½  
Organ Damage â—½  
Multiple Organ â—½  
High Mobility Group â—½  
Organ Injury â—½  
Cell Mediated Immunity â—½  
Functional Changes â—½  
Multiple Organs â—½  
Major Factors

Sepsis remains one of the leading causes of mortality in intensive care units, but there is a shortage of effective treatments. A dysregulated host immune response and multiple organ injury are major factors for the pathogenesis and progression of sepsis, which require specific mechanism and treatment. In the present study, we performed an intracerebroventricular (ICV) injection of BoxA, a specific antagonist of high-mobility group box 1 protein (HMGB1), in septic rats that were produced by cecal ligation and puncture surgery; we further assessed the functional changes of multiple organs and splenic T lymphocytes. We found that the inhibition of cerebral HMGB1 significantly alleviated multiple organ damage under septic exposure, including damage to the heart, liver, lungs, and kidneys; reversed the immune dysfunction of T cells; and increased the survival of septic rats. These data suggest that central HMGB1 might be a potential therapeutic target for septic challenge and that inhibition of brain HMGB1 can protect against multiple organ dysfunction induced by sepsis.

scholarly journals High-mobility group box-1 protein from CC10+ club cells promotes type 2 response in the later stage of respiratory syncytial virus infection

2019 â—½  
Vol 316 (1) â—½  
pp. L280-L290 â—½  
Author(s):  
Sisi Chen â—½  
Guangyuan Yu â—½  
Jun Xie â—½  
Wei Tang â—½  
Leiqiong Gao â—½  
...  
Keyword(s):  
Respiratory Syncytial Virus â—½  
High Mobility â—½  
Clinical Severity â—½  
High Mobility Group â—½  
Hmgb1 Protein â—½  
Club Cells â—½  
Hmgb1 Expression â—½  
Syncytial Virus â—½  
Tract Infections

The type 2 immune response, induced by infection of respiratory syncytial virus (RSV), has been linked to asthma development, but it remains unclear how the response is initiated. Here, we reported that the high-mobility group box-1 (HMGB1) protein promotes the type 2 response in the later stage of RSV infection. In mice, we found that type 2 cytokines were elevated in the later stages, which were strongly diminished after administration of anti-HMGB1 antibodies. Further investigation revealed that HMGB1 expression was localized to CC10+ club cells in the lung. In the clinic, levels of HMGB1 in nasopharyngeal aspirates in hospitalized infants with RSV bronchiolitis [median (interquartile range) 161.20 ng/ml (68.06–221.30)] were significantly higher than those without lower respiratory tract infections [21.94 ng/ml (12.12–59.82); P < 0.001]. Moreover, higher levels of HMGB1 correlated with clinical severity. These results reveal a link between viral infection and the asthma-like type 2 responses that are associated with long-term consequences.

scholarly journals High Mobility Group Box 1: a Novel Host Restriction Factor in Zika Virus Replication

2021 â—½  
Author(s):  
Kim-Ling Chin â—½  
Nurhafiza binti Zainal â—½  
Sing-Sin Sam â—½  
Pouya Hassandarvish â—½  
Rafidah Lani â—½  
...  
Keyword(s):  
Zika Virus â—½  
Severe Disease â—½  
High Mobility â—½  
High Mobility Group â—½  
Enzyme Linked Immunosorbent Assay â—½  
Dependent Manner â—½  
Zikv Infection â—½  
Hmgb1 Level â—½  
Antiviral Effects â—½  
Huh7 Cells

Abstract Neonatal microcephaly and adult Guillain-Barré syndrome are severe complications of Zika virus (ZIKV) infection. The robustly induced inflammatory cytokine expressions in ZIKV-infected patients may constitute a hallmark for severe disease. In the present study, the potential role of high mobility group box 1 protein (HMGB1) in ZIKV infection was investigated. HMGB1 protein expression was determined by the enzyme-linked immunosorbent assay (ELISA) and immunoblot assay. HMGB1’s role in ZIKV infection was also explored using treatment with dexamethasone, an immunomodulatory drug. Antiviral effects of dexamethasone treatment on both wild-typed (WT) and HMGB1-knockdown (shHMGB1) Huh7 cells were determined by the focus-forming assay. Results showed that the Huh7 cells were highly susceptible to ZIKV infection. The infection was found to induce HMGB1 nuclear-to-cytoplasmic translocation, resulting in a >99% increase in the cytosolic HMGB1 expression at 72h.p.i. The extracellular HMGB1 level was elevated in a time- and multiplicity of infection (MOI)- dependent manner. Dexamethasone 150 µM treatment of the ZIKV-infected cells reduced HMGB1 extracellular release in a dose-dependent manner, with a maximum reduction of 71 ± 5.84% (p < 0.01). The treatment also reduced virus titers by over 83 ± 0.50% (p < 0.01). The antiviral effects, however, was not observed in the dexamethasone-treated HMGB1-knockdown cells, suggesting the importance of the intracellular HMGB1 in ZIKV infection. Overall, these results suggest that translocation of HMGB1 occurred during ZIKV infection and inhibition of the translocation reduced ZIKV replication. These findings highlight the potential of developing therapeutics against ZIKV infection by affecting the translocation of HMGB1 from the nucleus to the cytoplasm.

scholarly journals High Mobility Group Box 1 Protein in Cerebral Thromboemboli

2021 â—½  
Vol 22 (20) â—½  
pp. 11276
Author(s):  
Fabian Essig â—½  
Lilith Babilon â—½  
Christoph Vollmuth â—½  
Alexander M. Kollikowski â—½  
Mirko Pham â—½  
...  
Keyword(s):  
Mechanical Thrombectomy â—½  
High Mobility â—½  
Large Vessel â—½  
High Mobility Group â—½  
Neutrophil Extracellular Trap â—½  
Spatial Proximity â—½  
Large Vessel Occlusion â—½  
Vessel Occlusion â—½  
Molecular Pattern â—½  
Hmgb1 Expression

High-mobility group box 1 protein (HMGB1) is a damage-associated molecular pattern (DAMP) involved in neutrophil extracellular trap (NET) formation and thrombosis. NETs are regularly found in cerebral thromboemboli. We here analyzed associated HMGB1 expression in human thromboemboli retrieved via mechanical thrombectomy from 37 stroke patients with large vessel occlusion. HMGB1 was detected in all thromboemboli, accounting for 1.7% (IQR 0.6–6.2%) of the total thromboemboli area and was found to be colocalized with neutrophils and NETs and in spatial proximity to platelets. Correlation analysis revealed that the detection of HMGB1 was strongly related to the number of neutrophils (r = 0.58, p = 0.0002) and platelets (r = 0.51, p = 0.001). Our results demonstrate that HMGB1 is a substantial constituent of thromboemboli causing large vessel occlusion stroke.

scholarly journals CO2Pneumoperitoneum Preservesβ-Arrestin 2 Content and Reduces High Mobility Group Box-1 (HMGB-1) Expression in an Animal Model of Peritonitis

10.1155/2015/160568 â—½  
2015 â—½  
Vol 2015 â—½  
pp. 1-7 â—½  
Author(s):  
Angela Simona Montalto â—½  
Alessandra Bitto â—½  
Letteria Minutoli â—½  
Pietro Impellizzeri â—½  
Gaetano Costa â—½  
...  
Keyword(s):  
Bacterial Load â—½  
Cecal Ligation â—½  
Signal Transduction Pathway â—½  
High Mobility â—½  
Receptor Activation â—½  
High Mobility Group â—½  
Male Rats â—½  
Toll Like Receptor â—½  
To Receive â—½  
Lung And Kidney

Laparoscopy (LS) has been shown to decrease the inflammatory sequelae of endotoxemia.β-arrestin 2 plays an important function in signal transduction pathway of TLR4. High mobility group box-1 (HMGB-1) is involved in the delayed systemic inflammatory response. We investigated the effects of CO2insufflation on liver, lung, and kidney expression of bothβ-arrestin 2 and HMGB-1 during sepsis. Cecal ligation and puncture (CLP) was performed in male rats and 6 h later the animals were randomly assigned to receive a CO2pneumoperitoneum or laparotomy. Animals were euthanized; liver, lung, and kidney were removed for the evaluation ofβ-arrestin 2 and HMGB-1 expression. Immunohistochemical detection of myeloperoxidase (MPO) was investigated in lung and liver and bacterial load was determined in the peritoneal fluid. CO2pneumoperitoneum reduced peritoneal bacterial load, increased the expression ofβ-arrestin 2, and blunted the expression of the potent proinflammatory HMGB-1 in liver, lung, and kidney compared with laparotomy. Liver and lung MPO was markedly reduced in rats subjected to LS compared with laparotomy. We believe that CO2exerts an early protective effect by reducing bacterial load and likely toll-like receptor activation which in turn leads to a preservedβ-arrestin 2 expression and a reduced HMGB-1 expression.

scholarly journals Acteoside improves survival in cecal ligation and puncture-induced septic mice via blocking of high mobility group box 1 release

Molecules and Cells â—½  
2013 â—½  
Vol 35 (4) â—½  
pp. 348-354 â—½  
Author(s):  
Eun Sun Seo â—½  
Bo Kang Oh â—½  
Jhang Ho Pak â—½  
Soon-Ho Yim â—½  
Sangilyandi Gurunathan â—½  
...  
Keyword(s):  
Cecal Ligation â—½  
High Mobility â—½  
High Mobility Group â—½  
Cecal Ligation And Puncture

scholarly journals Inhibitory Effect of Glycyrrhizin on the Phosphorylation and DNA-Binding Abilities of High Mobility Group Proteins 1 and 2 in Vitro.

10.1248/bpb.24.906 â—½  
2001 â—½  
Vol 24 (8) â—½  
pp. 906-911 â—½  
Author(s):  
Ryoko SAKAMOTO â—½  
Maiko OKANO â—½  
Hiroko TAKENA â—½  
Kenzo OHTSUKI
Keyword(s):  
Dna Binding â—½  
High Mobility â—½  
Inhibitory Effect â—½  
High Mobility Group â—½  
High Mobility Group Proteins

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

10.1093/abbs/gmx085 â—½  
2017 â—½  
Vol 49 (10) â—½  
pp. 907-915 â—½  
Author(s):  
Xin Wang â—½  
Renlingzi Zhang â—½  
Yao Tong â—½  
Xibing Ding â—½  
Shuqing Jin â—½  
...  
Keyword(s):  
Lung Injury â—½  
Protective Effect â—½  
High Mobility â—½  
High Mobility Group â—½  
Ventilation Induced Lung Injury

Penehyclidine hydrochloride inhibits the release of high-mobility group box 1 in lipopolysaccharide-activated RAW264.7 cells and cecal ligation and puncture–induced septic mice

2014 â—½  
Vol 186 (1) â—½  
pp. 310-317 â—½  
Author(s):  
Qiang Yang â—½  
Xiangge Liu â—½  
Zhongyan Yao â—½  
Shunhong Mao â—½  
Qianjie Wei â—½  
...  
Keyword(s):  
Cecal Ligation â—½  
High Mobility â—½  
High Mobility Group â—½  
Raw264.7 Cells â—½  
Cecal Ligation And Puncture â—½  
Penehyclidine Hydrochloride
Sign in / Sign up

Export Citation Format

Share Document