Effects of capsaicin on stress-induced duodenal injury

Ren, Jiangtao; Ojeas, Heri; Lightfoot, Stan; Harty, Richard F.

doi:10.3748/wjg.v4.isuppl2.49

Cited by 2 publications

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“…Failure of intestinal barrier function often occurs in many clinical conditions, including hemorrhage shock, severe burn injury, and the surgically critical illness, resulting in the increased intestinal permeability and subsequent translocation of bacteria or/and endotoxin from gut [8][9][10][11][12] . It is clear that increased gut permeability and bacteria with or without endotoxin translocation play a key role in the development of severe complications such as systemic inflammatory response syndrome (SIRS), sepsis, multiple organ dysfunction syndrome (MODS) and multiple organ failure (MOF) [13][14][15][16][17][18][19][20] .…”

Section: Introductionmentioning

confidence: 99%

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

Sun¹

2001

WJG

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AIM To explore the kinetic changes in plasma D(-)-lactate and lipopolysaccharide (LPS) levels, and investigate whether D(-)-lactate could be used as a marker of intestinal injury in rats following gut ischemia/ reperfusion, burn, and acute necrotizing pancreatitis (ANP).METHODS Three models were developed in rats: gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and ANP induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct. Plasma levels of D(-)-lactate in systemic circulation and LPS in portal circulation were measured by enzymaticspectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken for histological analysis.RESULTS One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D(-)-lactate and LPS levels, and there was a significant correlation between the plasma D(-)-lactate and LPS (r = 0.719, P<0.05). The plasma concentrations of D(-)-lactate and LPS increased significantly at 6h postburn, and there was also a remarkable correlation between them (r = 0.877, P<0.01). D(-)-lactate and LPS levels elevated significantly at 2h after ANP, with a similar significant correlation between the two levels (r =0.798, P<0.01). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were observed in all groups.CONCLUSION The changes of plasma D(-)-lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D(-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.Subject headings gut/injury; ischemia reperfusion/ blood; burn/blood; acute necrotizing pancreatitis/blood; D ( -)-lactate/blood; lipopolysaccharide/blood; intestinal permeability Sun XQ, Fu XB, Zhang R, Lü Y, Deng Q, Jiang XG, Sheng ZY. Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats. World J Gastroenterol, 2001;7(4):555-558

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Section: Introductionmentioning

confidence: 99%

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

Sun¹

2001

WJG

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“…Stress has been shown to induce gastric mucosal lesions and lower the effectiveness of the mucosa as a barrier [1][2][3][4][5][6] . In rats, gastric ulcers can be produced by cold-restraint stress [7][8][9] and it is frequently employed as a model for the study of the mechanisms of stress on ulcer formation.…”

Section: Introductionmentioning

confidence: 99%

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

Shen¹

2001

WJG

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AIM To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL·L -1 , i.g.) was used to induce gastric mucosa damage.RESULTS RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL·L -1 ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15±4.2)mm 2 was significantly lower (P<0.01) than the corresponding control (53.7± 8.1) mm 2 .CONCLUSION Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection. Subject headingssleep deprivation; heat shock proteins 70/biosynthesis; gastric mucosa; rats Shen XZ, Koo MWL, Cho CH. Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa. World J Gastroenterol, 2001;7(4):496-499

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Effects of capsaicin on stress-induced duodenal injury

Cited by 2 publications

References 0 publications

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

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