Melittin inhibits cerulein-induced acute pancreatitis via inhibition of the JNK pathway

Song, Yun; Bae, Gi‐Sang; Kim, Min-Sun; Park, Kyoung-Chel; Koo, Bon Soon; Kim, Byung‐Jin; Kim, Tae-Hyeon; Seo, Sang-Wan; Shin, Yong-Kook; Lee, Seung Ho; Song, Ho‐Joon; Park, Sung‐Joo

doi:10.1016/j.intimp.2011.08.020

Cited by 24 publications

(13 citation statements)

References 47 publications

(56 reference statements)

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“…It was also reported that PERK and phosphorylation of eIF2a were activated at an early stage (within 4 h) in cerulein-induced pancreatitis (31). In pancreatitis, excessive IRE1a activated the phosphorylation of JNK and other 'warning genes', such as p38 and NF-κB, which strongly responded to ER stress during AP injury, promoting transcription of various inflammatory genes and pancreatic neutrophil infiltration (32)(33)(34).…”

Section: Melatonin Attenuates the Inflammatory Response Via Inhibitinmentioning

confidence: 99%

Melatonin attenuates the inﬂammatory response via�inhibiting the C/EBP homologous protein-mediated pathway in taurocholate-induced acute pancreatitis

et al. 2018

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Acute pancreatitis (AP) is a serious disease characterized by the activation of trypsin, autodigestion, edemas, hemorrhages and necrosis. However, the mechanisms of regulating the apoptosis and inflammation of acinar cells in AP remain unclear. The endoplasmic reticulum (ER) stress-related molecule, c/EBP homologous protein (cHOP), has pro-apoptotic and pro-inflammatory properties, in addition to regulating ER stress responses. In the present study, a lentivirus-mediated RNA interference (RNAi) approach was used to specifically knockdown the expression of cHOP in the pancreatic tissue of Sprague-dawley rats to investigate the potential role of cHOP during AP, which was induced by the retrograde injection of 5% taurocholate into the biliopancreatic duct of rats. Pre-treatment with melatonin was further used to identify the potential anti-inflammatory mechanisms in AP. Pancreatic tissues were procured for western blot analysis, histological examination, reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining. ER stress was rapidly activated in the early stage and increased over time in the rat AP model. However, the silencing of cHOP expression markedly inhibited apoptosis and ER stress, reducing the activation of nuclear factor-κB and inflammation injury in AP. Melatonin also exhibited anti-inflammatory and apoptotic effects, and significantly decreased the expression of cHOP. Thus, it can be concluded that the cHOP-mediated pathway serves an important role in the development of AP, and that melatonin can reduce pancreatic damage via the inhibition of cHOP expression.

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Section: Melatonin Attenuates the Inflammatory Response Via Inhibitinmentioning

confidence: 99%

Melatonin attenuates the inﬂammatory response via�inhibiting the C/EBP homologous protein-mediated pathway in taurocholate-induced acute pancreatitis

et al. 2018

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“…26,27 Some studies concerning pancreatic injury have indicated that activated JNK and p38 strongly respond to ERS pathways through not only the release of the inflammatory cytokines TNF-α, IL-1 and IL-6 but also the increase in pancreatic neutrophil infiltration. 28,29 The activation of PERK and the phosphorylation of eIF2α have been observed at an early stage of caerulein-induced pancreatitis. 30,31 Moreover, the ERS process is associated with the activation of numerous genes and transcription factors, including ATF3.…”

Section: Ers and Apmentioning

confidence: 99%

“…IRE1α can also regulate other warning genes such as p38 MAPK and NF‐κB . Some studies concerning pancreatic injury have indicated that activated JNK and p38 strongly respond to ERS pathways through not only the release of the inflammatory cytokines TNF‐α, IL‐1 and IL‐6 but also the increase in pancreatic neutrophil infiltration . The activation of PERK and the phosphorylation of eIF2α have been observed at an early stage of caerulein‐induced pancreatitis …”

Section: Ers and Apmentioning

confidence: 99%

Endoplasmic reticulum stress is activated in acute pancreatitis

Chen

et al. 2016

J of Digest Diseases

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Endoplasmic reticulum (ER) is one of the most important cell organelles in the body, regulating protein synthesis, folding and aggregation. Endoplasmic reticulum stress (ERS) is a particular subcellular pathological process involving an imbalance of homeostasis and ER disorder. In the early stage of ERS, cells show a protective unfolded protein response that changes the cellular transcriptional and translational programs to alleviate the process. Therefore, a certain degree of ERS can activate the protective adaptation of cells, whereas sustained severe ERS triggers an apoptotic signal and leads to apoptosis. Acute pancreatitis is a disease caused by trypsin digestion of the pancreas, although the pathogenesis is not completely understood. However, a close association has been suggested between pancreatitis and ERS. This article reviewed relevant research advances and discussed the effect of ERS on the development and progression of acute pancreatitis.

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“…In most of the cases, the incidence of acute pancreatitis comprises of auto‐digestion of the pancreas by pancreatic zymogens which result in overwhelmed inflammatory response . The mortality rate of AP is severe when the condition progress to lung injury followed by multiple organ dysfunctions . The intricate balance of cytokine production relates the degree of tissue damage …”

Section: Introductionmentioning

confidence: 99%

“…[1] The mortality rate of AP is severe when the condition progress to lung injury followed by multiple organ dysfunctions. [2][3][4][5] The intricate balance of cytokine production relates the degree of tissue damage. [6][7][8] Though several mediators like tumour necrosis factoralpha (TNF-a), interleukin-1 beta (IL-1b) have been investigated for their prominent role in inflammation, other gaseous mediators which are also reported to play a modulatory role in inflammation like hydrogen sulfide (H 2 S), nitric oxide (NO) and carbon monoxide (CO) are less explored.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of methylsulfonylmethane in caerulein-induced acute pancreatitis and associated lung injury in mice

Velusamy

Tamizhselvi

2018

Journal of Pharmacy and Pharmacology

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Melittin inhibits cerulein-induced acute pancreatitis via inhibition of the JNK pathway

Cited by 24 publications

References 47 publications

Melatonin attenuates the inﬂammatory response via�inhibiting the C/EBP homologous protein-mediated pathway in taurocholate-induced acute pancreatitis

Melatonin attenuates the inﬂammatory response via�inhibiting the C/EBP homologous protein-mediated pathway in taurocholate-induced acute pancreatitis

Endoplasmic reticulum stress is activated in acute pancreatitis

Protective effect of methylsulfonylmethane in caerulein-induced acute pancreatitis and associated lung injury in mice

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