Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

Iwaya, Hitoshi; Fujii, Nobuyuki; Hagio, Masahito; Hara, Hiroshi; Ishizuka, Satoshi

doi:10.1271/bbb.130105

Cited by 13 publications

(9 citation statements)

References 33 publications

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“…Disease Activity Index is a cumulative index of ulcerative colitis to quantify body weight loss, rectal bleeding and stool consistency [67,68]. Another researcher reported that 1% DSS for 9 days and 2% DSS for 6 days minimum induces colitis in male wild type rats [69]. Some researchers have reported that chronic colitis is induced by 4% DSS for 6 days, followed by water for 6 days for three cycles in Sprague-Dawley rats [50].…”

Section: Chemical Induced Models Of Chronic Intestinal Inflammationmentioning

confidence: 99%

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Randhawa

Singh

et al. 2014

Korean J Physiol Pharmacol

357

310

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Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.

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Section: Chemical Induced Models Of Chronic Intestinal Inflammationmentioning

confidence: 99%

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Randhawa

Singh

et al. 2014

Korean J Physiol Pharmacol

357

310

View full text Add to dashboard Cite

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“…NASH is a liver inflammatory disease, sharing several features with atherosclerosis [ 248 ]. Besides atherosclerosis, sepsis, and NASH, DPP-4 inhibitors and GLP-1 analogs exert immunomodulatory effects in various models of chronic inflammatory diseases such as colitis [ 249 ], asthma [ 250 ], chronic obstructive lung disease (COPD) [ 251 ], and rheumatoid arthritis [ 252 ].…”

Section: Antioxidants 20—pleiotropic Antioxidant Effects Of Estabmentioning

confidence: 99%

Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease

Steven

Münzel

Daiber

2015

IJMS

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Cardiovascular disease is a leading cause of death and reduced quality of life worldwide. Arterial vessels are a primary target for endothelial dysfunction and atherosclerosis, which is accompanied or even driven by increased oxidative stress. Recent research in this field identified different sources of reactive oxygen and nitrogen species contributing to the pathogenesis of endothelial dysfunction. According to lessons from the past, improvement of endothelial function and prevention of cardiovascular disease by systemic, unspecific, oral antioxidant therapy are obviously too simplistic an approach. Source- and cell organelle-specific antioxidants as well as activators of intrinsic antioxidant defense systems might be more promising. Since basic research demonstrated the contribution of different inflammatory cells to vascular oxidative stress and clinical trials identified chronic inflammatory disorders as risk factors for cardiovascular events, atherosclerosis and cardiovascular disease are closely associated with inflammation. Therefore, modulation of the inflammatory response is a new and promising approach in the therapy of cardiovascular disease. Classical anti-inflammatory therapeutic compounds, but also established drugs with pleiotropic immunomodulatory abilities, demonstrated protective effects in various models of cardiovascular disease. However, results from ongoing clinical trials are needed to further evaluate the value of immunomodulation for the treatment of cardiovascular disease.

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“…Importantly, DPP-4 inhibition exerts immunosuppressive effects in various inflammation models, e.g., colitis [16], asthma [38] and rheumatoid arthritis [5]. Recently, we demonstrated that DPP-4 inhibition by linagliptin improved vascular dysfunction and oxidative stress levels in endotoxemic rats leading to significant reduction of infiltration of CD11b/c positive cells into the vessel wall and reduced adhesion of human monocytes and granulocytes to cultured endothelial cells [21].…”

Section: Introductionmentioning

confidence: 99%

Gliptin and GLP‐1 analog treatment improves survival and vascular inflammation/dysfunction in animals with lipopolysaccharide‐induced endotoxemia

et al. 2015

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Dipeptidyl peptidase (DPP)-4 inhibitors are used to treat hyperglycemia by increasing the incretin glucagon-like peptide-1 (GLP-1). Previous studies showed anti-inflammatory and antiatherosclerotic effects of DPP-4 inhibitors. Here, we compared the effects of linagliptin versus sitagliptin and liraglutide on survival and vascular function in animal models of endotoxic shock by prophylactic therapy and treatment after lipopolysaccharide (LPS) injection. Gliptins were administered either orally or subcutaneously: linagliptin (5 mg/kg/day), sitagliptin (50 mg/kg/day) or liraglutide (200 µg/kg/day). Endotoxic shock was induced by LPS injection (mice 17.5-20 mg/kg i.p., rats 10 mg/kg/day). Linagliptin and liraglutide treatment or DPP-4 knockout improved the survival of endotoxemic mice, while sitagliptin was ineffective. Linagliptin, liraglutide and sitagliptin ameliorated LPS-induced hypotension and vascular dysfunction in endotoxemic rats, suppressed inflammatory parameters such as whole blood nitrosyl-iron hemoglobin (leukocyte-inducible nitric oxide synthase activity) or aortic mRNA expression of markers of inflammation as well as whole blood and aortic reactive oxygen species formation. Hemostasis (tail bleeding time, activated partial thromboplastin time) was impaired in endotoxemic rats and recovered under cotreatment with linagliptin and liraglutide. Finally, the beneficial effects of linagliptin on vascular function and inflammatory parameters in endotoxemic mice were impaired in AMP-activated kinase (alpha1) knockout mice. The improved survival of endotoxemic animals and other data shown here may warrant further clinical evaluation of these drugs in patients with septic shock beyond the potential improvement of inflammatory complications in diabetic individuals with special emphasis on the role of AMP-activated kinase (alpha1) in the DPP-4/GLP-1 cascade.

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Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

Cited by 13 publications

References 33 publications

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease

Gliptin and GLP‐1 analog treatment improves survival and vascular inflammation/dysfunction in animals with lipopolysaccharide‐induced endotoxemia

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