The Prophylactic Effect of L-arginine in Acute Ischaemic Colitis in a Rat Model of Ischaemia/reperfusion Injury

Fotiadis, C; Adamis, S; Misiakos, Evangelos P.; Genetzakis, Michael; Antonakis, Pantelis; Tsekouras, Dimitrios; Gorgoulis, Vassilis G.; Zografos, Georgios; Papalois, Αpostolos; Fotinou, Marianthi; Περρέα, Δέσποινα

doi:10.1080/00015458.2007.11680039

Cited by 24 publications

(22 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similarly to glutamine discussed below, L-Arg is a "conditionally essential" amino acid for which the demand may exceed the supply under condition of catabolic stress or organ dysfunction. L-Arg supplementation attenuated tissue damage during acute ischemic colitis and promoted healing of intestinal mucosa (7, 8), and improved the symptoms of DSS-induced colitis in mice (9). Interestingly, L-Arg treatment resulted in increased ex vivo migration of colonic epithelial cells, thus suggesting an increased capacity for wound repair.…”

Section: Epithelial Transport Of Macronutrients In Ibdmentioning

confidence: 99%

Epithelial Transport in Inflammatory Bowel Diseases

Ghishan¹,

Kiela²

2014

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

The epithelium of the gastrointestinal tract is one of the most versatile tissues in the organism, responsible for providing a tight barrier between dietary and bacterial antigens and the mucosal and systemic immune system, while maintaining efficient digestive and absorptive processes to ensure adequate nutrient and energy supply. Inflammatory Bowel Diseases (IBD; Crohn’s disease and ulcerative colitis) are associated with a breakdown of both functions, which in some cases are clearly interrelated. In this updated literature review, we focus on the effects of intestinal inflammation and the associated immune mediators on selected aspects of the transepithelial transport of macro- and micronutrients. The mechanisms responsible for nutritional deficiencies are not always clear and could be related to decreased intake, malabsorption and excess losses. We summarize the known causes of nutrient deficiencies and the mechanism of IBD-associated diarrhea. We also overview the consequences of impaired epithelial transport, which infrequently transcend its primary purpose to affect the gut microbial ecology and epithelial integrity. While some of those regulatory mechanisms are relatively well established, more work needs to be done to determine how inflammatory cytokines can alter the transport process of nutrients across the gastrointestinal and renal epithelia.

show abstract

Section: Epithelial Transport Of Macronutrients In Ibdmentioning

confidence: 99%

Epithelial Transport in Inflammatory Bowel Diseases

Ghishan¹,

Kiela²

2014

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

show abstract

“…21 L-Arg supplementation attenuated the degree of tissue damage in intestinal ischemia and promoted healing of intestinal mucosa, in a rat model. 22 We have previously shown in the Citrobacter rodentium infection model of murine colitis that there is a significant decrease in the serum L-Arg concentration versus uninfected control mice, and that L-Arg supplementation is clinically beneficial. 23 Additionally, we have shown that L-Arg supplementation in an epithelial injury and repair model of murine colitis induced by dextran sulfate sodium (DSS), a heparin-like polysaccharide, leads to decreased body weight loss, mucosal permeability, and mortality.…”

Section: Introductionmentioning

confidence: 98%

L-Arginine Availability and Metabolism Is Altered in Ulcerative Colitis

Coburn

Horst

Allaman

et al. 2016

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

Background L-arginine (L-Arg) is the substrate for both inducible nitric oxide (NO) synthase (NOS2) and arginase (ARG) enzymes. L-Arg is actively transported into cells via cationic amino acid transporter (SLC7) proteins. We have linked L-Arg and arginase 1 activity to epithelial restitution. Our aim was to determine if L-Arg, related amino acids, and metabolic enzymes are altered in ulcerative colitis (UC). Methods Serum and colonic tissues were prospectively collected from 38 controls and 137 UC patients. Dietary intake, histologic injury, and clinical disease activity were assessed. Amino acid levels were measured by HPLC. mRNA levels were measured by real-time PCR. Colon tissue samples from 12 Crohn’s disease (CD) patients were obtained for comparison. Results Dietary intake of arginine and serum L-Arg levels were not different in UC patients versus controls. In active UC, tissue L-Arg was decreased, while L-citrulline (L-Cit) and the L-Cit/L-Arg ratio were increased. This pattern was also seen when paired involved (left) versus uninvolved (right) colon tissues in UC were assessed. In active UC, SLC7A2 and ARG1 mRNA levels were decreased, while ARG2 and NOS2 were increased. Similar alterations in mRNA expression occurred in tissues from CD patients. In involved UC, SLC7A2 and ARG1 mRNA levels were decreased, and NOS2 and ARG2 increased, when compared to uninvolved tissues. Conclusions UC patients exhibit diminished tissue L-Arg, likely attributable to decreased cellular uptake and increased consumption by NOS2. These findings combined with decreased ARG1 expression, indicate a pattern of dysregulated L-Arg availability and metabolism in UC.

show abstract

“…At 3 to 4 h after reperfusion, we carried out an absorption experiment of FD-4, and calculated AUC of 3 to 4 h after reperfusion (AUC [3][4]. Although the AUC 3-4 of FD-4 was significantly increased in a hanging-force-dependent manner during ischemia compared with that in the control condition, the rate of increase was smaller than that 0-1 h after reperfusion.…”

Section: Changes In Paracellular Permeability 3-4 H After Reperfusionmentioning

confidence: 84%

Effect of Aminoguanidine on Ischemia/Reperfusion Injury in Rat Small Intestine

Takizawa

Kitazato

Ishizaka

et al. 2011

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Ischemia/reperfusion (I/R) injury is induced by reactive oxygen species (ROS). During intestinal I/R, the amount of nitric oxide (NO), which is a ROS, is increased. In this study, we examined the protection against I/R injury by inhibition of NO generation. Wistar/ST rats were exposed to 1 h of ischemia, followed by reperfusion for 4 h. The rats were intravenously injected with 100 mg/kg aminoguanidine (AG), which is a selective inducible NO synthase (iNOS) inhibitor, for 5 min before ischemia. The increase in NO(2)(-) by intestinal I/R was significantly inhibited by AG 1 h after reperfusion. Moreover, the increase in area under curve of 0 to 1 h after reperfusion (AUC(0-1)) of paracellular marker was inhibited. However, 3 h after reperfusion, the survival ratio of rats was significantly decreased in the intestinal I/R condition with AG. The amount of NO(2)(-) and AUC of 3 to 4 h after reperfusion (AUC(3-4)) of paracellular marker in intestinal I/R groups were increased by AG compared with those in the I/R condition without AG 3 h after reperfusion. These data indicated that AG, which was given by single pre-administration, can clearly inhibit intestinal I/R injury 1 h after reperfusion. However, the injury occurs again 3 h after reperfusion and grows worse.

show abstract

The Prophylactic Effect of L-arginine in Acute Ischaemic Colitis in a Rat Model of Ischaemia/reperfusion Injury

Cited by 24 publications

References 0 publications

Epithelial Transport in Inflammatory Bowel Diseases

Epithelial Transport in Inflammatory Bowel Diseases

L-Arginine Availability and Metabolism Is Altered in Ulcerative Colitis

Effect of Aminoguanidine on Ischemia/Reperfusion Injury in Rat Small Intestine

Contact Info

Product

Resources

About