Synergistic effects of antibodies against high‐mobility group box 1 and tumor necrosis factor‐α antibodies on <scp>d</scp>‐(+)‐galactosamine hydrochloride/lipopolysaccharide‐induced acute liver failure

Wang, Wei; Sun, Li; Deng, Yonghao; Tang, Jie

doi:10.1111/febs.12132

Cited by 28 publications

(17 citation statements)

References 47 publications

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“…For example, TNF- α or TNF- α receptor-deficient mice was able to resist the challenge of GalN/LPS [29]. In later stage, attracted neutrophils and monocytes by inflammatory cytokines and chemokines generate massive ROS and protease, contributing to hepatocyte necrosis, which is characterized by increased plasma HMGB1 released from dysfunctional tissues [28, 30]. Therefore, we speculated that administration with cordycepin might be profitable for acute liver injury caused by GalN/LPS injection.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury

Zhong

Zhu

et al. 2017

Mediators of Inflammation

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As the major active ingredient of Cordyceps militaris, cordycepin (3′-deoxyadenosine) has been well documented to alleviate inflammation and oxidative stress both in vitro and in vivo. To explore the potential protective effect of cordycepin in fulminant hepatic failure, mice were pretreated with cordycepin for 3 weeks followed by D-galactosamine (GalN)/lipopolysaccharide (LPS) injection. Then we found cordycepin (200 mg/kg) administration elevated survival rate, improved liver function, and suppressed hepatocyte apoptosis and necrosis in mice with severe hepatic damage by GalN/LPS treatment. Further, cordycepin inhibited hepatic neutrophil and macrophage infiltration and prevented proinflammatory cytokine production possibly through suppressing TLR4 and NF-κB signaling transduction. The blockade of reactive oxygen species (ROS) and lipid peroxidation production by cordycepin was associated with the decrease of NAD(P)H oxidase (NOX) activity. Besides, cordycepin significantly prevented excessive autophagy induced by GalN/LPS in the liver. These data suggested that cordycepin could be a promising therapeutic agent for GalN/LPS-induced hepatotoxicity.

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Section: Discussionmentioning

confidence: 99%

The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury

Zhong

Zhu

et al. 2017

Mediators of Inflammation

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“…A partly humanized anti-HMGB1 monoclonal antibody attenuates acetaminophen hepatotoxicity and postinjury inflammation in mice [30]. HMGB1 is released into the serum at early stage of D-galactosamine/LPS-induced ALF, and HMGB1 acts synergistically with TNF- α to promote the inflammatory liver injury; this detrimental effect can be reversed by monoclonal antibodies against HMGB1 and TNF- α [31]. Inhibition of sphingosine kinase-1 ameliorates experimental ALF by reducing high-mobility group box 1 cytoplasmic translocation in liver cells [32].…”

Section: The Role Of Hmgb1 In Alfmentioning

confidence: 99%

HMGB1 and Extracellular Histones Significantly Contribute to Systemic Inflammation and Multiple Organ Failure in Acute Liver Failure

Yang

Zou

Tenhunen

et al. 2017

Mediators of Inflammation

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Acute liver failure (ALF) is the culmination of severe liver cell injury from a variety of causes. ALF occurs when the extent of hepatocyte death exceeds the hepatic regenerative capacity. ALF has a high mortality that is associated with multiple organ failure (MOF) and sepsis; however, the underlying mechanisms are still not clear. Emerging evidence shows that ALF patients/animals have high concentrations of circulating HMGB1, which can contribute to multiple organ injuries and mediate gut bacterial translocation (BT). BT triggers/induces systemic inflammatory responses syndrome (SIRS), which can lead to MOF in ALF. Blockade of HMGB1 significantly decreases BT and improves hepatocyte regeneration in experimental acute fatal liver injury. Therefore, HMGB1 seems to be an important factor that links BT and systemic inflammation in ALF. ALF patients/animals also have high levels of circulating histones, which might be the major mediators of systemic inflammation in patients with ALF. Extracellular histones kill endothelial cells and elicit immunostimulatory effect to induce multiple organ injuries. Neutralization of histones can attenuate acute liver, lung, and brain injuries. In conclusion, HMGB1 and histones play a significant role in inducing systemic inflammation and MOF in ALF.

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“…Monoclonal anti-HMGB1 neutralizing antibody (isotype IgG) derived from NZB/W mouse (HMGB1 Ab) (19,23,24) was gifted by the Institute of Biophysics, Chinese Academy of Science (Beijing, China). Of HMGB1 Ab, 200 mg were injected into recipient intraperitoneally (i.p.…”

Section: Hmgb1 Antibody Treatmentmentioning

confidence: 99%

HMGB1 Is Involved in Chronic Rejection of Cardiac Allograft via Promoting Inflammatory-Like mDCs

Zou

Yang

Gao

et al. 2014

American Journal of Transplantation

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Synergistic effects of antibodies against high‐mobility group box 1 and tumor necrosis factor‐α antibodies on d‐(+)‐galactosamine hydrochloride/lipopolysaccharide‐induced acute liver failure

Abstract: high-mobility group box 1 (HMGB1); lipopolysaccharide (LPS); synergistic effect; tumor necrosis factor-a (TNF-a) Correspondence

Cited by 28 publications

References 47 publications

The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury

The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury

HMGB1 and Extracellular Histones Significantly Contribute to Systemic Inflammation and Multiple Organ Failure in Acute Liver Failure

HMGB1 Is Involved in Chronic Rejection of Cardiac Allograft via Promoting Inflammatory-Like mDCs

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