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Page 1 od 41 rezultati
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Mitigates Experimental Colitis Through Inhibition of Intestinal Mucosal Inflammatory Responses via MEK-ERK Signaling
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N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an endogenous immunomodulatory peptide that is generated from thymosin β4 (Tβ4) through stepwise hydrolysis, involving meprin-α and prolyl endopeptidase (PREP). It is well acknowledged that AcSDKP exerts beneficial effects on multiple cardiovascular
Orally administered angiotensin-converting enzyme-inhibitors captopril and isoleucine-proline-proline have distinct effects on local renin-angiotensin system and corticosterone synthesis in dextran sulfate sodium-induced colitis in mice.
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The effects of angiotensin-converting enzyme (ACE) inhibition by an antihypertensive drug, captopril, and milk casein-derived ACE-inhibiting bioactive tripeptide isoleucine-proline-proline (Ile-Pro-Pro), on local renin-angiotensin system (RAS) and glucocorticoid production in the intestine were
Overexpression of Ste20-related proline/alanine-rich kinase exacerbates experimental colitis in mice.
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Inflammatory bowel disease, mainly Crohn's disease and ulcerative colitis, are characterized by epithelial barrier disruption and altered immune regulation. Colonic Ste20-like proline/alanine-rich kinase (SPAK) plays a role in intestinal inflammation, but its underlying mechanisms need to be
Nuclear factor-kappaB is a critical mediator of Ste20-like proline-/alanine-rich kinase regulation in intestinal inflammation.
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Inflammatory bowel disease (IBD) is thought to result from commensal flora, aberrant cellular stress, and genetic factors. Here we show that the expression of colonic Ste20-like proline-/alanine-rich kinase (SPAK) that lacks a PAPA box and an F-alpha helix loop is increased in patients with IBD. The
Arg72Pro polymorphism of p53 may predict poor response to medical treatment in ulcerative colitis.
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OBJECTIVE
Arg72Pro is a polymorphism commonly occurring in the proline-rich domain of Tp53. It can determine the development of different types of cancers, such as breast, lung, cervical, colorectal and hepatocellular carcinoma. Previous studies reported a correlation between Pro72 homozygosity and
A novel prodrug of 4'-geranyloxy-ferulic acid suppresses colitis-related colon carcinogenesis in mice.
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The inhibitory effects of a novel prodrug, 3-(4'-geranyloxy-3'-methoxyphenyl)-2-trans-propenoyl-L-alanyl-L-proline (GAP), of the secondary metabolite 4'-geranyloxy-3'-methoxyphenyl)-2-trans-propenoic acid (4'-geranyloxy-ferulic acid), on colon carcinogenesis was investigated using an azoxymetahen
A new model for the discrimination between ulcerative colitis and Crohn's disease.
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Distinguishing ulcerative colitis (UC) from Crohn's disease (CD) is sometimes difficult in a clinical setting. The purpose of this study was to identify a series of independent serum markers capable of distinguishing between UC and CD. 140 UC and 174 CD patients hospitalized at The First Affiliated
p53 codon 72 polymorphism in patients affected with ulcerative colitis.
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BACKGROUND
The p53 tumor suppressor protein plays a fundamental role in maintaining genomic integrity through its ability to arrest the cell cycle in G1 and induce apoptosis. The proapoptotic activity of p53 seems to be strictly related to proline-rich regions, homologous to the SH3 binding domain.
Dipeptidyl peptidase 4 inhibitor sitagliptin protected against dextran sulfate sodium-induced experimental colitis by potentiating the action of GLP-2.
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Dipeptidyl peptidase 4 (DPP4), a ubiquitously expressed protease that cleaves off the N-terminal dipeptide from proline and alanine on the penultimate position, has important roles in many physiological processes. In the present study, experimental colitis was induced in mice receiving 3% dextran
Gaudichaudione H Inhibits Inflammatory Responses in Macrophages and Dextran Sodium Sulfate-Induced Colitis in Mice.
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Macrophages-involved inflammation is considered to induce the damage in various diseases. Herein, novel therapeutics inhibiting over-activation of macrophages could prove an effective strategy to prevent inflammation-related diseases. Gaudichaudione H (GH), which is a natural small molecular
Abnormalities of jejunal mucosal enzymes in ulcerative colitis and Crohn's disease.
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Jejunal mucosal function and structure was examined in 31 patients with ulcerative colitis and 29 patients with Crohn's disease with ileal, ileocolonic or colonic involvement; A significant reduction of the specific activity of disaccharidases (lactase, sucrase and trehalase) in jejunal mucosal
Investigation of novel biomarkers for predicting the clinical course in patients with ulcerative colitis.
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BACKGROUND
The clinical course of ulcerative colitis (UC) is characterized by repeated episodes of relapse and remission. We hypothesized that biomarkers that help distinguish refractory UC patients who are in remission using strong anti-immunotherapy could contribute in preventing the overuse of
Knockout of Ste20-like proline/alanine-rich kinase (SPAK) attenuates intestinal inflammation in mice.
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Inflammatory bowel diseases are characterized by epithelial barrier disruption and alterations in immune regulation. Ste20-like proline/alanine-rich kinase (SPAK) plays a role in intestinal inflammation, but the underlying mechanisms need to be defined. Herein, SPAK knockout (KO) C57BL/6 mice
Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis.
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Overcoming adverse effects and selectively delivering drug to target cells are two major challenges in the treatment of ulcerative colitis (UC). Lysine-proline-valine (KPV), a naturally occurring tripeptide, has been shown to attenuate the inflammatory responses of colonic cells. Here, we loaded KPV
Effects of dietary tryptophan supplementation in the acetic acid-induced colitis mouse model.
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Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is strongly associated with intestinal immunity and the microbiome. Tryptophan (Trp) is an inflammatory inhibitor and modulator of the intestinal microflora. We explored the serum profile of
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