Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition

Severe acute pancreatitis (SAP) is a potentially lethal disease characterized by sudden onset, rapid progression,multiple organ failure and high mortality rate.[1-3] The underlying pathogenesis remains incompletely elucidated. As main anatomic and functional barrier, gut mucosa impairment is conside...

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Veröffentlicht in:Hepatobiliary & pancreatic diseases international 2017-08, Vol.16 (4), p.431-436
Hauptverfasser: Ning, Jian-Wen, Zhang, Yan, Yu, Mo-Sang, Gu, Meng-Li, Xu, Jia, Usman, Ali, Ji, Feng
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container_issue 4
container_start_page 431
container_title Hepatobiliary & pancreatic diseases international
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creator Ning, Jian-Wen
Zhang, Yan
Yu, Mo-Sang
Gu, Meng-Li
Xu, Jia
Usman, Ali
Ji, Feng
description Severe acute pancreatitis (SAP) is a potentially lethal disease characterized by sudden onset, rapid progression,multiple organ failure and high mortality rate.[1-3] The underlying pathogenesis remains incompletely elucidated. As main anatomic and functional barrier, gut mucosa impairment is considered one of the major pathologies in SAP,[4, 5] which will increase intestinal permeability, bacteria translocation as well as release of endotoxin, inflammatory mediators and cytokines(IL-1β, IL-18).[6]Caspase-1 (IL-1β-converting enzyme/ICE) is a common intracellular cysteine protease that converts the precursors of IL-1β and IL-18 into active cytokines.[7, 8]Blockade of caspase-1 suppresses inflammatory mediator expressions, such as IL-1β and IL-18, which will alleviate inflammation cascade reaction and ameliorate the overall severity and mortality of patients with SAP.[9, 10]
doi_str_mv 10.1016/S1499-3872(17)60041-9
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As main anatomic and functional barrier, gut mucosa impairment is considered one of the major pathologies in SAP,[4, 5] which will increase intestinal permeability, bacteria translocation as well as release of endotoxin, inflammatory mediators and cytokines(IL-1β, IL-18).[6]Caspase-1 (IL-1β-converting enzyme/ICE) is a common intracellular cysteine protease that converts the precursors of IL-1β and IL-18 into active cytokines.[7, 8]Blockade of caspase-1 suppresses inflammatory mediator expressions, such as IL-1β and IL-18, which will alleviate inflammation cascade reaction and ameliorate the overall severity and mortality of patients with SAP.[9, 10]</description><identifier>ISSN: 1499-3872</identifier><identifier>DOI: 10.1016/S1499-3872(17)60041-9</identifier><identifier>PMID: 28823375</identifier><language>eng</language><publisher>Singapore: Elsevier B.V</publisher><subject>acute ; Acute Disease ; Animals ; Caspase 1 - genetics ; Caspase 1 - metabolism ; Caspase Inhibitors - pharmacology ; caspase-1 inhibitor ; Disease Models, Animal ; emodin ; Emodin - pharmacology ; Inflammation Mediators - blood ; inhibitor ; Interleukin-18 - blood ; Interleukin-1beta - blood ; intestinal mucosa ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - enzymology ; Intestinal Mucosa - ultrastructure ; Male ; mucosa;emodin;caspase-1 ; Pancreas - drug effects ; Pancreas - metabolism ; Pancreas - ultrastructure ; Pancreatitis - chemically induced ; Pancreatitis - drug therapy ; Pancreatitis - enzymology ; Pancreatitis - pathology ; pancreatitis;intestinal ; Rats, Sprague-Dawley ; severe ; severe acute pancreatitis ; Severity of Illness Index ; Signal Transduction - drug effects ; Taurocholic Acid</subject><ispartof>Hepatobiliary &amp; pancreatic diseases international, 2017-08, Vol.16 (4), p.431-436</ispartof><rights>2017 The Editorial Board of Hepatobiliary &amp; Pancreatic Diseases International</rights><rights>Copyright © 2017 The Editorial Board of Hepatobiliary &amp; Pancreatic Diseases International. 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As main anatomic and functional barrier, gut mucosa impairment is considered one of the major pathologies in SAP,[4, 5] which will increase intestinal permeability, bacteria translocation as well as release of endotoxin, inflammatory mediators and cytokines(IL-1β, IL-18).[6]Caspase-1 (IL-1β-converting enzyme/ICE) is a common intracellular cysteine protease that converts the precursors of IL-1β and IL-18 into active cytokines.[7, 8]Blockade of caspase-1 suppresses inflammatory mediator expressions, such as IL-1β and IL-18, which will alleviate inflammation cascade reaction and ameliorate the overall severity and mortality of patients with SAP.[9, 10]</abstract><cop>Singapore</cop><pub>Elsevier B.V</pub><pmid>28823375</pmid><doi>10.1016/S1499-3872(17)60041-9</doi><tpages>6</tpages></addata></record>
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source MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects acute
Acute Disease
Animals
Caspase 1 - genetics
Caspase 1 - metabolism
Caspase Inhibitors - pharmacology
caspase-1 inhibitor
Disease Models, Animal
emodin
Emodin - pharmacology
Inflammation Mediators - blood
inhibitor
Interleukin-18 - blood
Interleukin-1beta - blood
intestinal mucosa
Intestinal Mucosa - drug effects
Intestinal Mucosa - enzymology
Intestinal Mucosa - ultrastructure
Male
mucosa
emodin
caspase-1
Pancreas - drug effects
Pancreas - metabolism
Pancreas - ultrastructure
Pancreatitis - chemically induced
Pancreatitis - drug therapy
Pancreatitis - enzymology
Pancreatitis - pathology
pancreatitis
intestinal
Rats, Sprague-Dawley
severe
severe acute pancreatitis
Severity of Illness Index
Signal Transduction - drug effects
Taurocholic Acid
title Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition
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