High-mobility group box 1 protein and its role in severe acute pancreatitis

Shen, Xiao

doi:10.3748/wjg.v21.i5.1424

Cited by 57 publications

(66 citation statements)

References 109 publications

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“…Extracellular HMGB1, one of the families of non-histone nuclear proteins, is already known as a novel pro-inflammatory cytokine in humans. In the last decade, many studies have claimed a positive relationship between extracellular HMGB1 expression and SAP severity [19]. Cyclooxygenase (COX), has two isoforms: COX-1 and COX-2, is a key enzyme in the synthesis of prostaglandins from arachidonic acid [20].…”

Section: Discussionmentioning

confidence: 99%

Emodin diminishes immune stress in rats with severe acute pancreatitis

Jin¹,

Zhang²,

Chen³

et al. 2018

biomedicalresearch

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Objectives: The aim was to observe the immune stress in rats with Severe Acute Pancreatitis (SAP) and diminish by emodin. Methods: Rats were divided into four groups: sham operation group (SO), SAP model group (SAP), emodin treatment group (ET), and two times dose emodin treatment group (HT). Samples of blood, terminal ileum and lung were harvested on 6 h, 12 h, 18 h and 24 h for examination. Serum amylase, and high-mobility group box 1 (HMGB 1), cyclooxygenase-2 (COX-2), and peroxisome proliferator activated receptor gamma-γ (PPAR-γ) in terminal ileum and lung was determined. Results: The values for emodin treated showed distinctly treatment effect, with lower levels of serum amylase, HMGB 1 and COX-2 on 12, 18 and 24 h and higher levels of PPAR-γ in the ET and HT groups compared with the SAP group on four time-points. The levels of detection indicators in the ET group were quite different from the HT group, with higher levels of serum amylase, HMGB 1 and COX-2 on 12, 18 and 24 h and lower expression of PPAR-γ on each time points. Conclusions: Emodin can diminish immune stress in rats with SAP. The strategy of two times may be a better therapeutic effect.

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Section: Discussionmentioning

confidence: 99%

Emodin diminishes immune stress in rats with severe acute pancreatitis

Jin¹,

Zhang²,

Chen³

et al. 2018

biomedicalresearch

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“…HMGB1 is a single peptide chain consisting of 215 amino acid residues with a molecular weight of ~30 kDa (30). It is an evolutionarily conserved nuclear protein in all mammals and is expressed in virtually all types of cells (31).…”

Section: Discussionmentioning

confidence: 99%

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response

Meiqing

et al. 2016

Experimental and Therapeutic Medicine

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The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective effects remains unclear. The aim of the present study was to investigate the mechanism underlying the protective effects of picroside II on I/R-induced myocardial injury. Adult male Sprague-Dawley rats underwent 1 h left coronary artery occlusion followed by 3 h reperfusion. Picroside II was administered (10 mg/kg) via the tail vein 30 min prior to left coronary artery occlusion. The results revealed that pretreatment of picroside II could significantly alleviate I/R-induced myocardial injury concomitantly with a decrease in inflammatory factor production. In addition, picroside II was also able to decrease high mobility group box 1 (HMGB1) expression, and release and downregulate the expression of the receptor for advanced glycation end products (RAGE), toll-like receptor (TLR)-2 and TLR-4. Furthermore, picroside II was able to inhibit nuclear factor-κB (NF-κB) activation. The results indicated that the protective effect of picroside II on I/R-induced myocardial injury was associated, at least partly, with inhibition of the inflammatory response by suppressing the HMGB1-RAGE/TLR-2/TLR-4-NF-κB signaling pathway.

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“…During SAP, the concentrations of both early (TNF-α, IL-6) and late inflammatory cytokines are significantly increased [6, 10–13], these cytokines play a significant role in the pathogenesis of SAP [6, 12]. The late inflammatory cytokine HMGB1 is particularly important because extracellular HMGB1 can aggravate the pancreatic inflammatory process [14] and HMGB1 can also contribute to multiple distant organ injuries in the following experimental models as well: HMGB1 contributes to liver injury in ischemia-reperfusion [15]. Exogenous HMGB1 injection is able to induce liver injury in normal mice [16].…”

Section: Ep Ameliorates Severe Acute Pancreatitis (Sap) and Attenuatementioning

confidence: 99%

“…Therefore, the gut is thought to act as the starter of SIRS [29] and HMGB1 may be an important factor that links gut barrier dysfunction and MODS during SAP. EP (40 mg/kg was intraperitoneally injected every 6 h for 48 h) can ameliorate SAP related multiple organ injuries [6, 10, 11] at least partly because EP not only reduces the inflammation in these organs [6, 10, 11], but also inhibits nearly 90% of the hepatic tissue HMGB1 to release [12] and other related cells to release HMGB1 [10, 12], thereby decreases the circulating HMGB1 level in SAP [10, 14]. Thus, HMGB1 is an important factor that not only directly contributes to multiple organ injuries, but also mediates gut BT to trigger/induce systemic inflammation/sepsis, the latter can lead to MODS.…”

Section: Ep Ameliorates Severe Acute Pancreatitis (Sap) and Attenuatementioning

confidence: 99%

“…Thus, HMGB1 is an important factor that not only directly contributes to multiple organ injuries, but also mediates gut BT to trigger/induce systemic inflammation/sepsis, the latter can lead to MODS. Currently, the circulating HMGB1 level is thought to be reliable to predict the severity of SAP [10, 14], this is likely because HMGB1 is linked to multiple organ injuries during SAP [10, 12, 14], the liver is an important source of circulating HMGB1 [12], and the circulating HMGB1 level could reflect the severity of liver injury, which is one of the important parameters for diagnosing SAP [6, 12]. SAP associated BT was reduced by 90% following EP treatment [6] breaking the link between BT and MODS.…”

Section: Ep Ameliorates Severe Acute Pancreatitis (Sap) and Attenuatementioning

confidence: 99%

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Ethyl pyruvate is a novel anti-inflammatory agent to treat multiple inflammatory organ injuries

2016

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Ethyl pyruvate (EP) is a simple derivative of pyruvic acid, which is an important endogenous metabolite that can scavenge reactive oxygen species (ROS). Treatment with EP is able to ameliorate systemic inflammation and multiple organ dysfunctions in multiple animal models, such as acute pancreatitis, alcoholic liver injury, acute respiratory distress syndrome (ARDS), acute viral myocarditis, acute kidney injury and sepsis. Recent studies have demonstrated that prolonged treatment with EP can ameliorate experimental ulcerative colitis and slow multiple tumor growth. It has become evident that EP has pharmacological anti-inflammatory effect to inhibit multiple early inflammatory cytokines and the late inflammatory cytokine HMGB1 release, and the anti-tumor activity is likely associated with its anti-inflammatory effect. EP has been tested in human volunteers and in a clinical trial of patients undergoing cardiac surgery in USA and shown to be safe at clinical relevant doses, even though EP fails to improve outcome of the heart surgery, EP is still a promising agent to treat patients with multiple inflammatory organ injuries and the other clinical trials are on the way. This review focuses on how EP is able to ameliorate multiple organ injuries and summarize recently published EP investigations. Graphical AbstractThe targets of the anti-inflammatory agent EP

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High-mobility group box 1 protein and its role in severe acute pancreatitis

Cited by 57 publications

References 109 publications

Emodin diminishes immune stress in rats with severe acute pancreatitis

Emodin diminishes immune stress in rats with severe acute pancreatitis

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response

Ethyl pyruvate is a novel anti-inflammatory agent to treat multiple inflammatory organ injuries

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