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C Crone J Frokjaer-Jensen JJ Friedman O Christensen 《The Journal of general physiology》1978,71(2):195-220
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Scanlan BJ Tuft B Elfrey JE Smith A Zhao A Morimoto M Chmielinska JJ Tejero-Taldo MI Mak IuT Weglicki WB Shea-Donohue T 《Molecular and cellular biochemistry》2007,306(1-2):59-69
The aim of this study was to determine the effect of magnesium deficiency on small intestinal morphology and function. Rats
were assigned to 4 groups and placed on magnesium sufficient or deficient diet for 1 or 3 weeks. Infiltration of neutrophils
and mucosal injury were assessed in stained sections of small intestine. Magnesium deficiency alone induced a significant
increase in neutrophil infiltration and increased vascular ICAM-1 expression, in the absence of changes in mucosal injury
or expression of proinflammatory mediators. Magnesium deficiency was associated with hyposecretory epithelial cell responses
and vascular macromolecular leak in the small intestine and lung, which was attributed partly to reduced expression of NOS-3.
To determine the effect of hypomagnesmia on the intestinal responses to a known oxidative stress, groups of rats were randomized
to either sham operation or superior mesenteric artery occlusion for 10 (non-injurious) or 30 (injurious) minutes followed
by a 1- or 4-hour reperfusion period. In response to mesenteric ischemia/reperfusion, deficient rats showed exaggerated PMN
influx, but similar mucosal injury. Intestinal ischemia in sufficient animals induced vascular macromolecular leak in the
small intestine and lung at 4 hours of reperfusion, with levels similar to those observed in untreated deficient rats. Acute
magnesium repletion of deficient rats 24 h before surgery attenuated the exaggerated inflammation in deficient rats. These
data show that magnesium deficiency induced a subclinical inflammation in the small intestine in the absence of mucosal injury,
but with significant functional changes in local and remote organs and increased sensitivity to oxidative stress.
The opinions contained herein are those of the authors and are not to be construed as official policy or reflecting the views
of the Department of Defense 相似文献
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Chmielinska JJ Tejero-Taldo MI Mak IT Weglicki WB 《Molecular and cellular biochemistry》2005,278(1-2):53-57
Substance P is elevated in plasma and in other tissues during Mg-deficiency, and was found localised to neuronal C-fibres
of cardiac and intestinal tissues, where it could promote neurogenic inflammation. Plasma prostaglandin E2 (PGE2), indicative of systemic inflammation, rose significantly (≥4 fold, p<0.01) after 1 week and remained elevated through week 2 and 3 in rat on the Mg-deficient (MgD) diet. Concomitantly, total
blood glutathione decreased by 50%. Immunohistochemical staining for endotoxin (lipopolysaccaride, LPS) receptor, CD14 was
prominent in macrophage-type cells in intestinal tissue; more importantly, cardiac tissue revealed both CD11b (monocyte/macrophage
surface protein) and CD14 positive cells after 3 weeks in rats on MgD diet. Western blot analysis indicated a significant
increase in the endotoxin receptor protein level in the 3 week MgD hearts. Since CD14 is known to be up-regulated in cells
exposed to LPS, these observations suggest that prolonged Mg-deficiency results in increased intestinal permeability to bacterial
products that induce the endotoxin receptor in cells localized to myocardial and intestinal tissues. These CD14 positive cells
may amplify the cardiomyopathic inflammatory process by stimulating TNF-α and other pro-inflammatory cytokines. (Mol Cell
Biochem 278: 53–57, 2005) 相似文献
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Lipoteichoic acid is an important microbe-associated molecular pattern of Lactobacillus rhamnosus GG
Claes Ingmar JJ Segers Marijke E Verhoeven Tine LA Dusselier Michiel Sels Bert F De Keersmaecker Sigrid CJ Vanderleyden Jos Lebeer Sarah 《Microbial cell factories》2012,11(1):1-8