Expression of apoptosis-related proteins in rat with induced colitis

D’Argenio, Giuseppe; Farrace, Maria Grazia; Cosenza, V.; Ritis, Francesca De; Valle, Nicola Della; Manguso, Francesco; Piacentini, Mauro

doi:10.1007/s00384-004-0585-5

Cited by 12 publications

(6 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IBD evoke a damage‐repair process accompanied by the activation of apoptotic genes. Previous studies have shown significant apoptosis in colonic epithelial cells during mild inflammation induced by TNBS, and it is suggested that expression of apoptosis markers is related to the degree of colitis ( Yue et al ., 2001 ; D'Argenio et al ., 2004 ). In addition, deregulated apoptosis seems to be a major cause of the impaired barrier function, leading to the invasion of pathogenic microorganisms, and to an increase of leukocyte survival with exacerbation of the disease ( Yue et al ., 2001 ).…”

Section: Discussionmentioning

confidence: 99%

The effects of resveratrol, a phytoalexin derived from red wines, on chronic inflammation induced in an experimentally induced colitis model

Martín

Villegas

Sánchéz-Hidalgo

et al. 2006

British J Pharmacology

217

127

View full text Add to dashboard Cite

1 Neutrophil infiltration, proinflammatory cytokines, eicosanoid generation and oxidative stress have been implicated in colitis. Resveratrol is a polyphenolic compound found in grapes and wine, with multiple pharmacological actions, including anti-inflammatory, antioxidant, antitumour and immunomodulatory activities. In a previous report, we documented that resveratrol decreases the degree of inflammation associated with acute experimental colonic inflammation, but its effects on chronic experimental colitis remain undetermined. 2 The aim of this research was to investigate the effects of resveratrol on the chronic colonic injury caused by intracolonic instillation of trinitrobenzenesulphonic acid (TNBS) in rats. The inflammatory response was assessed by histology and myeloperoxidase activity. Tumour necrosis factor alpha (TNF-a) production, histological and histochemical analysis of the lesions were also carried out. We determined the production of prostaglandin (PG) E 2 and D 2 in colon mucosa, as well as cyclooxygenase (COX)-1 and -2 and nuclear transcription factor NF-kappa B (NF-kB) p65 protein expression. Finally, since resveratrol has been found to modulate apoptosis, we intended to elucidate its effects on colonic mucosa under chronic inflammatory conditions. 3 Resveratrol (10 mg kg À1 day À1) significantly attenuated the damage score and corrected the disturbances in morphology associated to injury. In addition, the degree of neutrophil infiltration and the levels of TNF-a were significantly ameliorated. Resveratrol did not modify PGD 2 levels but returned the decreased PGE 2 values to basal levels and also reduced COX-2 and the NF-kB p65 protein expression. Furthermore, treatment of rats with resveratrol caused a significant increase of TNBS-induced apoptosis in colonic cells. 4 In conclusion, resveratrol reduces the damage in chronic experimentally induced colitis, alleviates the oxidative events, returns PGE 2 production to basal levels and stimulates apoptosis in colonic cells.

show abstract

Section: Discussionmentioning

confidence: 99%

The effects of resveratrol, a phytoalexin derived from red wines, on chronic inflammation induced in an experimentally induced colitis model

Martín

Villegas

Sánchéz-Hidalgo

et al. 2006

British J Pharmacology

217

127

View full text Add to dashboard Cite

show abstract

“…Our finding that the specific inhibitor of K ϩ channels 48F10 can prevent apoptosis in enterocytes may have an important clinical implication. Intestinal disorders such as ulcerative colitis (3,15,44), coeliac disease (2,22,25), necrotizing enterocolitis (18,28), and microvillus inclusion disease (10) are associated with increased levels of enterocyte apoptosis. Specific inhibitors of enterocyte K ϩ channels may be useful in preventing or modulating gut barrier failure associated with these inflammatory conditions.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of apoptosis in enterocytes by blockade of potassium channels

Grishin¹,

Ford²,

Jin³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Apoptosis plays an important role in maintaining the balance between proliferation and cell loss in the intestinal epithelium. Apoptosis rates may increase in intestinal pathologies such as inflammatory bowel disease and necrotizing enterocolitis, suggesting pharmacological prevention of apoptosis as a therapy for these conditions. Here, we explore the feasibility of this approach using the rat epithelial cell line IEC-6 as a model. On the basis of the known role of K+ efflux in apoptosis in various cell types, we hypothesized that K+ efflux is essential for apoptosis in enterocytes and that pharmacological blockade of this efflux would inhibit apoptosis. By probing intracellular [K+] with the K+-sensitive fluorescent dye and measuring the efflux of 86Rb+, we found that apoptosis-inducing treatment with the proteasome inhibitor MG-132 leads to a twofold increase in K+ efflux from IEC-6 cells. Blockade of K+ efflux with tetraethylammonium, 4-aminopyridine, stromatoxin, chromanol 293B, and the recently described K+ channel inhibitor 48F10 prevents DNA fragmentation, caspase activation, release of cytochrome c from mitochondria, and loss of mitochondrial membrane potential. Thus K+ efflux occurs early in the apoptotic program and is required for the execution of later events. Apoptotic K+ efflux critically depends on activation of p38 MAPK. These results demonstrate for the first time the requirement of K+ channel-mediated K+ efflux for progression of apoptosis in enterocytes and suggest the use of K+ channel blockers to prevent apoptotic cell loss occurring in intestinal pathologies.

show abstract

“…The epithelial cell injury in inflamed colonic mucosa in IBD is due to the apoptotic cell death [26]. p53 is one of the major regulators in apoptosis and its protein level increases in the colon mucosa of IBD [26].…”

Section: Discussionmentioning

confidence: 99%

“…p53 is one of the major regulators in apoptosis and its protein level increases in the colon mucosa of IBD [26]. Increased apoptosis in DSS-induced colitis may bring a destruction of the epithelial barrier function and facilitate the mucosal invasion of harmful intestinal bacteria, which leads to the chronic phase of colitis.…”

Section: Discussionmentioning

confidence: 99%

Ethanol Extract ofCordyceps militarisGrown on Germinated Soybeans Attenuates Dextran-Sodium-Sulfate- (DSS-) Induced Colitis by Suppressing the Expression of Matrix Metalloproteinases and Inflammatory Mediators

Park

2013

BioMed Research International

View full text Add to dashboard Cite

The effect of Cordyceps militaris (CM) grown on germinated soybeans (GSC) in the inflammatory bowel disease (IBD) model was studied. To demonstrate the preventive effect of GSC extract in a dextran-sodium-sulfate- (DSS-) induced acute colitis mouse model, GSC was administered 2 days before DSS coadministration. GSC significantly suppressed DSS-induced disease activity index (DAI) as well as histopathological scores, compared to control or CM-treated group. To elucidate the anti-IBD activity of GSC, we checked the level of matrix metalloproteinases (MMPs) and inflammatory mediators. GSC extract decreased the level of MMP-3 and -9 mRNAs and p53 proteins. The level and activity of LPS-induced MMP-9 were reduced in GSC-treated RAW264.7 cells. It also attenuated the level of inducible nitric oxide synthase (iNOS) and tumor necrosis factor- (TNF-) α mRNAs both in colon tissue and in macrophage cells. These results suggest that GSC can be applied as a protective agent against IBDs.

show abstract

Expression of apoptosis-related proteins in rat with induced colitis

Cited by 12 publications

References 44 publications

The effects of resveratrol, a phytoalexin derived from red wines, on chronic inflammation induced in an experimentally induced colitis model

The effects of resveratrol, a phytoalexin derived from red wines, on chronic inflammation induced in an experimentally induced colitis model

Attenuation of apoptosis in enterocytes by blockade of potassium channels

Ethanol Extract ofCordyceps militarisGrown on Germinated Soybeans Attenuates Dextran-Sodium-Sulfate- (DSS-) Induced Colitis by Suppressing the Expression of Matrix Metalloproteinases and Inflammatory Mediators

Contact Info

Product

Resources

About