Angiotensin Converting Enzyme-Inhibitor Reduces Colitis Severity in an IL-10 Knockout Model

Sueyoshi, Ryo; Ignatoski, Kathleen M. Woods; Daignault, Stephanie; Okawada, Manabu; Teitelbaum, Daniel H.

doi:10.1007/s10620-013-2825-4

Cited by 27 publications

(35 citation statements)

References 50 publications

(65 reference statements)

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“…In vivo administration of the ACE inhibitor enalaprilate has been proven to reduce weight loss and histological damage in murine dextran sulfate sodium (DSS)-induced colitis [ 146 ]. ACE inhibitor treatment was also effective in spontaneous colitis of IL-10-deficient mice [ 147 ] and this finding has been confirmed by other studies [ 148 , 149 ].…”

Section: Reviewsupporting

confidence: 71%

Medical therapy of stricturing Crohn’s disease: what the gut can learn from other organs - a systematic review

Bettenworth

Rieder

2014

Fibrogenesis Tissue Repair

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Crohn’s disease (CD) is a chronic remitting and relapsing disease. Fibrostenosing complications such as intestinal strictures, stenosis and ultimately obstruction are some of its most common long-term complications. Despite recent advances in the pathophysiological understanding of CD and a significant improvement of anti-inflammatory therapeutics, medical therapy for stricturing CD is still inadequate. No specific anti-fibrotic therapy exists and the incidence rate of strictures has essentially remained unchanged. Therefore, the current therapy of established fibrotic strictures comprises mainly endoscopic dilation as well as surgical approaches. However, these treatment options are associated with major complications as well as high recurrence rates. Thus, a specific anti-fibrotic therapy for CD is urgently needed. Importantly, there is now a growing body of evidence for prevention as well as effective medical treatment of fibrotic diseases of other organs such as the skin, lung, kidney and liver. In face of the similarity of molecular mechanisms of fibrogenesis across these organs, translation of therapeutic approaches from other fibrotic diseases to the intestine appears to be a promising treatment strategy. In particular transforming growth factor beta (TGF-β) neutralization, selective tyrosine kinase inhibitors, blockade of components of the renin-angiotensin system, IL-13 inhibitors and mammalian target of rapamycin (mTOR) inhibitors have emerged as potential drug candidates for anti-fibrotic therapy and may retard progression or even reverse established intestinal fibrosis. However, major challenges have to be overcome in the translation of novel anti-fibrotics into intestinal fibrosis therapy, such as the development of appropriate biomarkers that predict the development and accurately monitor therapeutic responses. Future clinical studies are a prerequisite to evaluate the optimal timing for anti-fibrotic treatment approaches, to elucidate the best routes of application, and to evaluate the potential of drug candidates to reach the ultimate goal: the prevention or reversal of established fibrosis and strictures in CD patients.

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Section: Reviewsupporting

confidence: 71%

Medical therapy of stricturing Crohn’s disease: what the gut can learn from other organs - a systematic review

Bettenworth

Rieder

2014

Fibrogenesis Tissue Repair

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“…Spencer et al (2007) have reported that enalaprilat treatment reduced the severity of DSS-induced colitis in mice and reduced epithelial cell apoptosis, possibly through suppressing TNF-α mRNA and reducing the ratio of proapoptotic Bax to antiapoptotic Bcl-2. Likewise, enalaprilat was shown to be effective in reducing disease severity in an IL-10 knockout colitis model, which was minimally augmented by prednisolone (Sueyoshi et al, 2013).…”

mentioning

confidence: 98%

The potential therapeutic use of renin–angiotensin system inhibitors in the treatment of inflammatory diseases

Ranjbar

Shafiee

Hesari

et al. 2018

Journal Cellular Physiology

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Inflammation is a normal part of the immune response to injury or infection but its dysregulation promotes the development of inflammatory diseases, which cause considerable human suffering. Nonsteroidal anti-inflammatory agents are the most commonly prescribed agents for the treatment of inflammatory diseases, but they are accompanied by a broad range of side effects, including gastrointestinal and cardiovascular events. The renin-angiotensin system (RAS) is traditionally known for its role in blood pressure regulation. However, there is increasing evidence that RAS signaling is also involved in the inflammatory response associated with several disease states. Angiotensin II increases blood pressure by binding to angiotensin type 1 (AT ) receptor, and direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors and AT receptor blockers (ARBs) are clinically used as antihypertensive agents. Recent data suggest that these drugs also have anti-inflammatory effects. Therefore, this review summarizes these recent findings for the efficacy of two of the most widely used antihypertensive drug classes, ACE inhibitors and ARBs, to reduce or treat inflammatory diseases such as atherosclerosis, arthritis, steatohepatitis, colitis, pancreatitis, and nephritis.

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“…23,24 In inflammation-based disorders, treatment with ACEI helps to control the inflammatory response and alleviate the tissue injury. 7,9,11 Previous studies have found that exposure to LPS significantly activated the RAS and increased the concentration of angiotensin II in plasma. 25,26 In the present study, we found that administration of captopril, a representative ACEI, attenuated LPS/GalN-induced fulminant liver injury and decreased the mortality of the mice with experimental acute hepatic failure.…”

Section: Discussionmentioning

confidence: 99%

The angiotensin-converting enzyme inhibitor captopril rescues mice from endotoxin-induced lethal hepatitis

Jiang

Yao

et al. 2016

Innate Immun

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The renin-angiotensin system is classically regarded as a crucial regulator of circulatory homeostasis, but recent studies also revealed its pro-inflammatory roles. The beneficial effects of the angiotensin-converting enzyme inhibitor (ACEI) in severe inflammatory injury in the lung and heart have been previously reported, but its potential effects on lethal hepatitis were unknown. In this study, a mouse model with LPS/d-galactosamine (GalN)-induced fulminant hepatitis were used to test the protective potential of captopril, a representative ACEI. The results indicated that treatment with captopril significantly decreased the plasma level of alanine aminotransferase and aspartate aminotransferase, alleviated the histopathological damage of the liver tissue and improve the survival rate of LPS/GalN-challenged mice. These effects were accompanied by reduced mRNA levels of TNF-α and IL-6 in the liver, and decreased protein level of TNF-α and IL-6 in the plasma. In addition, the activation of caspases 3, 8 and 9, and the presence of TUNEL-positive apoptotic cells, were also suppressed by captopril treatment. The above evidence suggested that the renin-angiotensin system might be involved in the development of LPS/GalN-induced fulminant hepatitis and ACEI might have potential value in lethal hepatitis.

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Angiotensin Converting Enzyme-Inhibitor Reduces Colitis Severity in an IL-10 Knockout Model

Cited by 27 publications

References 50 publications

Medical therapy of stricturing Crohn’s disease: what the gut can learn from other organs - a systematic review

Medical therapy of stricturing Crohn’s disease: what the gut can learn from other organs - a systematic review

The potential therapeutic use of renin–angiotensin system inhibitors in the treatment of inflammatory diseases

The angiotensin-converting enzyme inhibitor captopril rescues mice from endotoxin-induced lethal hepatitis

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