Breakdown of Intestinal Mucosa Via Accelerated Apoptosis Increases Intestinal Permeability in Experimental Severe Acute Pancreatitis

Yasuda, Takeo; Takeyama, Yoshifumi; Ueda, Takashi; Shinzeki, Makoto; Sawa, Hirofumi; Nakajima, Takahiro; Kuroda, Yoshikazu

doi:10.1016/j.jss.2006.02.050

Cited by 76 publications

(62 citation statements)

References 45 publications

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“…Apoptosis participates in AP onset [16] . The apoptosis of pancreatic acinar cell might be a reaction beneficial to the body after the occurrence of pancreatitis [17,18] . Both necrosis and apoptosis are death modes of injured cells [19] .…”

Section: Group (T /H) Pancreas Head Pancreas Tail 3 H 6 H 12 H 3 H 6 mentioning

confidence: 99%

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Zhang

Chen²,

Hu³

et al. 2007

WJG

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AIM:To investigate the influence of high dose of dexamethasone on inflammatory mediators and apoptosis of rats with severe acute pancreatitis (SAP).METHODS: SAP rats were randomly assigned to the model group and treatment group while the normal rats were assigned to the sham operation group. The mortality, ascite volumes, ascites/body weight ratio and pancreas pathological changes of all rats were observed at 3, 6 and 12 h after operation. Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor (TNF-α), phospholipase A2 (PLA2) and IL-6 in serum were also determined. The microarray sections of their pancreatic tissues were prepared, terminal transferase dUTP nick end labeling (TUNEL) staining was performed and apoptotic indexes were calculated. RESULTS:There was no marked difference between treatment group and model group in survival. The contents of amylase and endotoxin in plasma and contents of TNF-α, PLA2 and IL-6 in serum, ascite volumes, ascites/body weight ratio and pancreas pathological scores were all lower in treatment group than in model group to different extents at different time

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Section: Group (T /H) Pancreas Head Pancreas Tail 3 H 6 H 12 H 3 H 6 mentioning

confidence: 99%

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Zhang

Chen²,

Hu³

et al. 2007

WJG

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“…Inflammatory cells, particularly neutrophils accumulate in this region and increase the release of free oxygen radicals, inflammatory response, and worsen the ischemic effect [2,17]. Damage of the mucosal integrity leads to an increase in intestinal permeability and damage in interstitial Cajal cells and myenteric neurons causes ileus progressing through endotoxemia and bacterial translocation [4,[17][18][19]. Moreover, apparently MMP-9 related changes also occur in the intestinal capillary endothelial barrier [20].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Erythropoietin on Intestinal Damage Developed Secondary to Experimental Acute Pancreatitis

M¹

2012

Pancreat Disorders Ther

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“…Therefore excessive apoptosis is a cause of IMB dysfunction and endotoxemia in SPA. [19,20] While the apoptosis is regulated by many genes, the bcl-2 genetic family is the primary gene which controls the apoptosis. The bcl-2 genetic family involves two kinds: the gene of inhibiting the apoptosis, such as bcl-2, bcl-x, bcl-w, etc., and the gene of promoting the apoptosis, such as bax, bad, bak, etc.…”

Section: Disscussionmentioning

confidence: 99%

Protective effect of exogenous IGF-I on the intestinal mucosal barrier in rats with severe acute pancreatitis

Wang¹,

Wang²,

Zhang³

et al. 2012

World Journal of Emergency Medicine

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BACKGROUND:Severe acute pancreatitis (SAP) can result in intestinal mucosal barrier (IMB) dysfunction. This study was undertaken to demonstrate the effect of IGF-I on the intestinal mucosal barrier in rats with SAP and its possible mechanisms.METHODS: Seventy-two male Wistar rats were randomly divided into three groups: a sham operation (SO group, n=24), a SAP group not treated with IGF-I (SAP group, n=24), and a SAP group treated with IGF-I (IGF-I group, n=24). SAP was induced in the rats by injecting 5.0% sodium taurocholate into the biliary-pancreatic duct. The SO rats were given an infusion of normal saline instead. The rats in the IGF-I group underwent the SAP procedure and were given a subcutaneous injection of IGF-I at 30 minutes before the operation and at 3 hours after the operation. Eight rats in each group were sacrificed at 6, 12 and 24 hours after operation. Apoptosis of mucosal cells in the small intestine was determined by TUNEL. The levels of endotoxin and DAO and serum amylase were also measured. Pathologic changes in the small intestine were monitored. Changes of bax and bcl-2 mRNA expression in the small intestine were determined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS:The levels of serum amylase were lower in the IGF-I group than in the SAP group at all three time points (P<0.05). The levels of endotoxin in the IGF-I group were higher than those in the SAP group at 6 hours, but lower in the IGF-I group than in the SAP group at 12 and 24 hours (P<0.05). The levels of diamine oxidase were higher in the IGF-I group at 6 hours but lower than those in the SAP group at 12 and 24 hours. The pathological score of the small intestine was lower in the IGF-I group than in the SAP group, and the difference was statistically signifi cant at 12 and 24 hours. The pathologic changes observed under electron microscopy were better in the IGF-I group than those in the SAP group. The apoptosis index of intestinal epithelial cells was significantly decreased in the IGF-I group compared with the SAP group. Compared with the SO group, the mRNA expression levels of bax were increased at each time point in the SAP group, and were significantly decreased in the IGF-I group as compared with the SAP group at each time point (P<0.05). The expression levels of bcl-2 were weak and not different between the SO group and the SAP group (P>0.05). They were significantly increased in the IGF-I group versus the SO and SAP groups (P<0.05). The ratio of bax and bcl-2 mRNA expression levels at each time point in the SAP group were signifi cantly higher than those in the SO group, but they were obviously decreased in the IGF-I group.CONCLUSIONS: Exogenous IGF-I seems to protect mucosal cells in the small intestine against SAP-induced apoptosis and could alleviate SAP-induced injury of the intestinal mucosa. The underlying mechanisms include enhanced mRNA expression of bcl-2 and inhibition of bax mRNA expression.

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Breakdown of Intestinal Mucosa Via Accelerated Apoptosis Increases Intestinal Permeability in Experimental Severe Acute Pancreatitis

Cited by 76 publications

References 45 publications

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

The Effect of Erythropoietin on Intestinal Damage Developed Secondary to Experimental Acute Pancreatitis

Protective effect of exogenous IGF-I on the intestinal mucosal barrier in rats with severe acute pancreatitis

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