The effect of angiotensin-converting enzyme inhibitors on experimental colitis in rats

Jahovic, Nermina; Ercan, Feríha; Gedik, Nursal; Yüksel, Meral; Şener, Göksel; Ali̇can, İnci̇

doi:10.1016/j.regpep.2005.03.009

Cited by 36 publications

(53 citation statements)

References 38 publications

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“…These investigators failed to see an improvement in the histology with lisinopril, but saw improvement with captopril. Additionally, they noted a diminution of the serum levels of TNF-α (58). While the observations made by these recent publications confirm many of the findings of our work, they do not completely address the potential mechanism by which inhibition of the RAS acts to prevent colitis.…”

Section: Discussioncontrasting

confidence: 53%

Reduced Severity of a Mouse Colitis Model with Angiotensin Converting Enzyme Inhibition

et al. 2007

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Ulcerative colitis is characterized by elevated rates of epithelial cell apoptosis, and an up-regulation of pro-apoptotic cytokines including tumor necrosis factor alpha (TNF-α). Recently, angiotensin converting enzyme (ACE) has been shown to promote apoptosis. In addition, pharmacologic ACE inhibition (ACE-I) both prevents apoptosis and reduces TNF-α expression in vitro. We hypothesized that ACE-I, using enalaprilat, would decrease colonic epithelial cell apoptosis and reduce colitis severity in the dextran sulfate sodium (DSS)-induced colitis model in mice. We assessed the severity of colitis, and colonic epithelial cell apoptosis, after administration of DSS. Mice were given either daily ACE-I treatment or daily placebo. ACE-I treatment markedly improved clinical outcomes. In addition, ACE-I treatment significantly reduced the maximum histopathologic colitis grade. ACE-I also dramatically reduced the epithelial apoptotic rate. To investigate the mechanism by which ACE-I reduced apoptosis; we measured TNF-α, Bcl-2, and Bax expression. TNF-α mRNA was significantly lower with ACE-I treatment compared to placebo at every time point; as was the ratio of Bax to Bcl-2. We conclude that ACE-I reduces the severity of DSS-induced colitis and reduces epithelial cell apoptosis.

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Section: Discussioncontrasting

confidence: 53%

Reduced Severity of a Mouse Colitis Model with Angiotensin Converting Enzyme Inhibition

et al. 2007

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“…Wengrower et al, demonstrated that prophylactic administration of Captopril in TNBS colitis could reduce damages scores and fibrosis after 21 days, as well as the levels of Ang II and TGF-beta [13]. On the other hand treatment with the same inhibitor administered after the induction of acute colitis did not show significant benefits in the observed lesions at the dose tested [45].…”

Section: Discussionmentioning

confidence: 99%

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

Santiago

Rivera

Ferder

et al. 2008

Regulatory Peptides

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Little is known about the effects of the proinflammatory hormone Angiotensin II (Ang II) in inflammatory bowel disease. The aim of this study was to evaluate the effect of Valsartan (Diovan), an Ang II receptor antagonist, in two models of colitis.METHODS-Colitis was induced in Sprague-Dawley rats by administration of trinitrobenzene sulfonic acid (TNBS; 30mg in 50% ETOH ic) or 5% Dextran Sulphate Sodium (DSS) in drinking water ad libitum for 5 days. Valsartan was administered orally in drinking water (160mg/L) during thirty days prior to the induction of the colitis, and for 5 days after. All animals were evaluated for weight change, diarrhea, myeloperoxidase activity, macroscopic and microscopic damage. Cytokine levels in the colon were measured by ELISA, real time RT-PCR and immunohistochemistry.RESULTS-In the TNBS model, Valsartan reduced the macroscopic damage score, significantly decreased the microscopic damage (p<0.01), and accelerated weight gain after colitis. In the DSS colitis model, Valsartan treated animals had less diarrhea and microscopic damage. Valsartan reduced the protein levels of TGFβ (p<0.05), and IL-18 in the TNBS model, and led to over-expression of IL-10 mRNA in the DSS model.CONCLUSION-These data demonstrate a possible anti-inflammatory effect for Valsartan in colitis.

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“…In parallel, elevation in Ang II expression in colon mucosa was also demonstrated in an animal model of trinitrobenzene sulphonic acid (TNBS)-induced experimental colitis. These changes were prevented by interfering with angiotensinogen gene expression (angiotensinogen defi cient mice) or pharmacological blockade of Ang II or its receptor by ACE inhibitor and ARB, respectively [9][10][11].…”

Section: Discussionmentioning

confidence: 99%

“…The studies addressing the role of RAS indicate that interfering with RAS function either by using ACE inhibitors or AT1 specifi c Ang II receptor blockers (ARB) attenuates infl ammatory response with respect to pro-infl ammatory cytokine production [9][10][11]. Similar observations were also made employing AT1a receptor defi cient mice [2,[12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 94%

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

et al. 2008

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The effect of angiotensin-converting enzyme inhibitors on experimental colitis in rats

Cited by 36 publications

References 38 publications

Reduced Severity of a Mouse Colitis Model with Angiotensin Converting Enzyme Inhibition

Reduced Severity of a Mouse Colitis Model with Angiotensin Converting Enzyme Inhibition

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

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