Journals / Turkish Journal of Gastroenterology / 2012 / Cilt: 23 - Sayı: 6

Sıçanlarda oluşturulan deneysel kolit modelinde glukagon benzeri peptid 2 nin bakteriyel translokasyon üzerine etkisi

Effects of glucagon-like peptide-2 on bacterial translocation in rat models of colitis

Pages
691–698
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Our results indicate that glucagon-like peptide-2 is a potential agent for treating colitis; however, extensive trials are needed to confirm our results.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/aims: The aim of this trial was to study the role of glucagon-like peptide-2 in reducing bacterial translocation by virtue of its anti-inflammatory effects and ability to decrease intestinal permeability in rat models of inflammatory bowel diseases.
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Key Findings & Data:To our knowledge, this is the first study of the effectiveness of glucagon-like peptide-2 on bacterial translocation, in treating an experimental colitis model.
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Conclusion & Impact:Our results indicate that glucagon-like peptide-2 is a potential agent for treating colitis; however, extensive trials are needed to confirm our results.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Background/aims: The aim of this trial was to study the role of glucagon-like peptide-2 in reducing bacterial translocation by virtue of its anti-inflammatory effects and ability to decrease intestinal permeability in rat models of inflammatory bowel diseases. On the basis of our results and those of other recent studies, we suggest a new treatment modality for colitis. To our knowledge, this is the first study of the effectiveness of glucagon-like peptide-2 on bacterial translocation, in treating an experimental colitis model. Methods: Rats were randomized into 3 groups of 7 rats each-the control group, colitis group, and treatment group. On the 7th day after induction of colitis, the levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin were measured. Tissue samples were obtained from the liver, spleen, and mesenteric lymph nodes for evaluating bacterial translocation. Results: Bacterial translocation in samples of the liver, spleen, mesenteric lymph nodes, and portal and systemic blood obtained from the treatment group was lower than that in samples obtained from the colitis group (p<0.05). The levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin in the treatment group were significantly lower than those in the colitis group (p<0.05). Conclusions: In experimental colitis models, which were induced using trinitrobenzene sulfonic acid in ethanol, glucagon-like peptide-2 treatment reduced inflammation and bacterial translocation from the intestinal mucosa. Our results indicate that glucagon-like peptide-2 is a potential agent for treating colitis; however, extensive trials are needed to confirm our results.

Özet

Amaç: Bu çalışmada glukagon benzeri peptid 2nin inflamatuar barsak hastalıklarında gösterdiği antiinflamatuvar etki ve intestinal permeabiliteyi azaltma yönündeki etkisinin, bakteriyel translokasyon üzerinde doğuracağı muhtemel düşüşün araştırılması ve bu çalışmanın doğuracağı sonuçlar ışığında, kolit tedavisinde kullanılabilecek yeni bir tedavi modalitesinin literatür desteği altı nda fakat yeni bir konu olarak tartışmaya sunulması amaçlanmaktadır. Bu açıdan çalışmamız, kolit modelinde glukagon benzeri peptid 2nin bakteriyel translokasyon üzerindeki etkinliğini araştırmayı amaçlayan ilk çalışmadır. Gereç ve Yöntem: Gruplar randomize olarak her biri 7şer ratdan oluşan kontrol, kolit ve tedavi olmak üzere 3e ayrıldı. Kolit oluşturulduktan sonraki 7. günde doku düzeyinde myeloperoksidaz, serumda ise tümör nekroz faktör alfa, plazma endotoksin düzeylerine bakıldı. Bakteriyel translokasyonu değerlendirmek için doku kültürü amacıyla karaciğer, dalak, mezenterik lenf nodlarından doku örneklemeleri yapıldı. Bulgular: Kolit grubuyla karşılaştırıldığında, glukagon benzeri peptid 2 ile tedavi grubunda karaciğer, dalak, mezenterik lenf nodları, portal ve sistemik kanda bakteriyel translokasyon azalmıştı (p<0.05). Tedavi grubunda doku myeloperoksidaz, serum tümör nekroz faktör alfa ve plazma endotoksin düzeyleri kolit grubuna göre belirgin şekilde düşüktü (p<0.05). Sonuç: Deneysel olarak oluşturulmuş kolit modelinde uygulanan glukagon benzeri peptid 2, barsak mukozasında gelişmiş inflamasyonu ve bakteriyel translokasyonu belirgin düzeyde azaltmıştır. Buradan hareketle kolit tedavisi için glukagon benzeri peptid 2nin de yeni ve umut vadeden bir ajan olarak gözönüne alınarak, konu hakkında daha kapsamlı ve geniş tabanlı araştırmalar yapılmasının bir gereklilik olduğuna inanıyoruz.

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Cite This Article

HALAÇLAR, B., AĞAÇ, A. A., AKCAN, A. C., Ay, A., ÖZ, B., ARSLAN, E. (2012). Sıçanlarda oluşturulan deneysel kolit modelinde glukagon benzeri peptid 2 nin bakteriyel translokasyon üzerine etkisi. Turkish Journal of Gastroenterology, Cilt: 23 - Sayı: 6, 691–698. https://ajindex.com/articles/409679

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References (15)

  1. Fink MP. Ethyl pyruvate: a novel anti-inflammatory agent. J Intern Med 2007; 261: 349-62
  2. Salahudeen AK, Clark EC, Nath KA. Hydrogen peroxide– induced renal injury. A protective role for pyruvate in vitro and in vivo. J Clin Invest 1991; 88: 1886-93
  3. Mouzaoui S, Rahim I, Djerdjouri B. Aminoguanidine and curcumin attenuated tumor necrosis factor (TNF)-α-induced oxidative stress, colitis and hepatotoxicity in mice. Int Immunopharmacol 2011; 10: 20-9
  4. Hamouda HE, Zakaria SS, Ismail SA, et al. p53 antibodies, metallothioneins, and oxidative stress markers in chronic ulcerative colitis with dysplasia. World J Gastroenterol 2011; 17: 2417-23
  5. Akcan A, Kucuk C, Sozuer E. Melatonin reduces bacterial translocation and apoptosis in trinitrobenzene sulphonic acid–induced colitis of rats. World J Gastroenterol 2008; 14: 918-24
  6. Bertevello PL, Logullo AF, Nonogaki S. Immunohistochemical assessment of mucosal cytokine profile in acetic acid experimental colitis. Clinics (Sao Paulo) 2005; 60: 277-86
  7. Yamamoto M, Yoshizaki K, Kishimoto T. IL–6 is required for the development of Th1 cell–mediated murine colitis. J Immunol 2000; 164: 4878-82
  8. Krawisz JE, Sharon P, Stenson WF. Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity. Assessment of inflammation in rat and hamster models. Gastroenterology 1984; 87: 1344-50
  9. Dincer Y, Erzin Y, Himmetoglu S. Oxidative DNA damage and antioxidant activity in patients with inflammatory bowel disease. Dig Dis Sci 2007; 52: 1636-41
  10. Andres PG, Friedman LS. Epidemiology and the natural course of inflammatory bowel disease. Gastroenterol Clin North Am 1999; 28: 255-81
  11. Loftus EV Jr, Sandborn WJ. Epidemiology of inflammatory bowel disease. Gastroenterol Clin North Am 2002; 31: 1-20
  12. Akcan A, Muhtaroglu S, Akgun H. Ameliorative effects of bombesin and neurotensin on trinitrobenzene sulphonic acid–induced colitis, oxidative damage and apoptosis in rats. World J Gastroenterol 2008; 14: 1222-30
  13. Wallace JL, Le T, Carter L. Hapten–induced chronic colitis in the rat: alternatives to trinitrobenzene sulfonic acid. J Pharmacol Toxicol Methods 1995; 33: 237-9
  14. Shibata Y, Taruishi M, Ashida T. Experimental ileitis in dogs and colitis in rats with trinitrobenzene sulphonic acidcolonoscopic and histopathologic studies. Gastroenterol Jpn 1993; 28: 518-27
  15. Ardizzone S, Bianchi Porro G. Inflammatory bowel disease: new insights into pathogenesis and treatment. J Intern Med