L-glutamine enemas attenuate mucosal injury in experimental colitis

Kaya, Ekrem; Gür, Esma; Özgüç, Halil; Bayer, Ahmet; Tokyay, Rifat

doi:10.1007/bf02238577

Cited by 28 publications

(17 citation statements)

References 49 publications

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“…Oral glutamine feeding of patients with CD for 4 weeks failed to improve the intestinal permeability in two randomized studies [28,29]. As opposed to systemic glutamine supplementation, topical application may mask circulating inflammatory cells from the immune-enhancing effect of glutamine and support mucosal healing in colitic disease, at least if administered before induction of colitis [24,26,27].…”

Section: Discussionmentioning

confidence: 96%

“…Furthermore, glutamine has been shown to be of benefit in methotrexate-induced enterocolitis [19,20] and to protect the intestinal mucosa from radiation injury [21,22]. Enteral glutamine feeding in experimental colitis, however, yielded conflicting results [23][24][25][26][27]. A glutamine-enriched polymeric diet in Crohn's disease (CD) failed to improve the intestinal permeability [28,29] and even deteriorated the clinical disease activity in pediatric patients [30].…”

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confidence: 99%

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Low Intestinal Glutamine Level and Low Glutaminase Activity in Crohn’s Disease: A Rational for Glutamine Supplementation?

et al. 2006

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Intestinal glutamine utilization is integral to mucosal regeneration. We analyzed the systemic and intestinal glutamine status in Crohn's disease (CD) and evaluated the therapeutic effect of glutamine supplementation in an animal model of ileitis. In CD, glutamine concentrations were decreased systemically and in noninflamed and inflamed ileal/colonic mucosa. Mucosal glutaminase activities were depressed in the ileum independent of inflammation but were not different from controls in the colon. In experimental ileitis, oral glutamine feeding prevented macroscopic inflammation, enhanced ileal and colonic glutaminase activities above controls, and normalized the intestinal glutathione redox status. However, glutamine supplementation enhanced myeloperoxidase activity along the gastrointestinal tract and potentiated lipid peroxidation in the colon. In conclusion, glutamine metabolism is impaired in CD. In experimental ileitis, glutamine supplementation prevents inflammatory tissue damage. In the colon, however, which does not use glutamine as its principal energy source, immune enhancement of inflammatory cells by glutamine increases oxidative tissue injury.

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Section: Discussionmentioning

confidence: 96%

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confidence: 99%

Low Intestinal Glutamine Level and Low Glutaminase Activity in Crohn’s Disease: A Rational for Glutamine Supplementation?

et al. 2006

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“…Therefore, it was determined that AA may have caused oxidative stress by leading to a marked increase in MDA levels in the colon tissue. MDA is the toxic end-product of lipid peroxidation, and reflects the level of lipid peroxidation in the tissue; hence its common usage as a marker of lipid peroxidation (31). MDA is secreted due to the toxic effects of active free oxygen radicals.…”

Section: Discussionmentioning

confidence: 99%

Effects of dexpanthenol on acetic acid-induced colitis in rats

Çağın

Parlakpınar

Vardı

et al. 2016

Experimental and Therapeutic Medicine

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While the pathogenesis of acetic acid (AA)-induced colitis is unclear, reactive oxygen species are considered to have a significant effect. The aim of the present study was to elucidate the therapeutic potential of dexpanthenol (Dxp) on the amelioration of colitis in rats. Group I (n=8; control group) was intrarectally administered 1 ml saline solution (0.9%); group II [n=8; AA] was administered 4% AA into the colon via the rectum as a single dose for three consecutive days; group III (n=8; AA + Dxp) was administered AA at the same dosage as group II from day 4, and a single dose of Dxp was administered intraperitoneally; and group IV (n=8; Dxp) was administered Dxp similarly to Group III. Oxidative stress and colonic damage were assessed via biochemical and histologic examination methods. AA treatment led to an increase in oxidative parameters and a decrease in antioxidant systems. Histopathological examination showed that AA treatment caused tissue injury and increased caspase-3 activity in the distal colon and triggered apoptosis. Dxp treatment caused biochemical and histopathological improvements, indicating that Dxp may have an anti-oxidant effect in colitis; therefore, Dxp may be a potential therapeutic agent for the amelioration of IBD.

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“…These findings suggest that NAC treatment had beneficial effects by reducing the severity of colonic inflammation. Many antioxidant agents have been investigated to prevent the colitis due to oxidant exposure e.g., Zolimid and AEOL11201 (Choudhary et al 2001), L-glutamine (Kaya et al 1999), melatonin (Pentney and Bubenik 1995) and ascorbat (Simmonds et al 1999). Also, beneficial effects of a polysaccharide "angelica sinensis" have been reported in trinitrobenzene sulfonic acid (TNBS) and ethanol-induced experimental colitis ).…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of N-Acetylcysteine on Acetic Acid-Induced Colitis in Rats

Çetinkaya¹,

Bülbüloğlu²,

Kurutaş³

et al. 2005

Tohoku J. Exp. Med.

100

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Ulcerative colitis is a chronic recurrent inflammatory bowel disease in which oxidative stress has been implicated. The aim of the present study was to evaluate possible protective effects of N-acetylcysteine against acetic acid-induced colitis in a rat model. Rats were administered intrarectal saline (control group) or acetic acid (colitis model group). Rats with acetic acid-induced colitis were treated by intraperitoneal or intrarectal administration of N-acetylcysteine (500 mg/ kg) (treated group). Another series of rats were pre-treated by intraperitoneal or intrarectal administration of N-acetylcysteine, then administered intrarectal acetic acid (pre-treated group). The degree of tissue injuries was assessed by macroscopical and histopathological scores of the colonic mucosa. Malondialdehyde, myeloperoxidase, reduced glutathione, superoxide dismutase, and catalase levels were measured in tissue extracts of the dissected colon. Administration of N-acetylcysteine intraperitoneally or intrarectally ameliorated macroscopic score alterations produced by acetic acid in treated groups. In addition, microscopical improvement was observed in all N-acetylcysteine-treated rats compared to untreated animals with colitis. In the colonic tissues of the acetic acid-induced colitis, myeloperoxidase activity and malondialdehyde levels were elevated, while the reduced glutathione levels and superoxide dismutase and catalase activities were decreased. However, intraperitoneal or intrarectal treatment with N-acetylcysteine reversed these parameters, compared to the untreated colitis group. Notably, intrarectal administration of N-acetylcysteine elevated the reduced glutathione levels more markedly compared to the other treatment groups. Superoxide dismutase levels were increased in intraperitoneally or intrarectally N-acetylcysteine-treated groups significantly compared to the control, colitis and pre-treated groups. But there was no significant increase in catalase activity. In conclusion, N-acetylcysteine could be beneficial as a complementary agent in treatment of ulcerative colitis.N-acetylcysteine; colitis; reactive oxygen species; acetic acid; GSH

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L-glutamine enemas attenuate mucosal injury in experimental colitis

Cited by 28 publications

References 49 publications

Low Intestinal Glutamine Level and Low Glutaminase Activity in Crohn’s Disease: A Rational for Glutamine Supplementation?

Low Intestinal Glutamine Level and Low Glutaminase Activity in Crohn’s Disease: A Rational for Glutamine Supplementation?

Effects of dexpanthenol on acetic acid-induced colitis in rats

Beneficial Effects of N-Acetylcysteine on Acetic Acid-Induced Colitis in Rats

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