Journals / Erciyes Medical Journal / 2015 / Cilt: 37 - Sayı: 4

Possible Activation of the Immune System by Chronic Peripheral Nesfatin-1 Application at the Acute Phase of Ischemia/Reperfusion Injury

Pages
143–147
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

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

This effect of nesfatin-1 may also increase the rejection of grafts during transplantation period

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Organ transplantation is one of the clinical scenarios involving ischemia and reperfusion process.
📊
Key Findings & Data:Nesfatin-1 is a peptide involved in the regulation of homeostasis and has anti-inflammatory as well as anti-ischemic properties.
💡
Conclusion & Impact:This effect of nesfatin-1 may also increase the rejection of grafts during transplantation period
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Organ transplantation is one of the clinical scenarios involving ischemia and reperfusion process. Ischemia/reperfusion is the pivotal mechanism of organ injury during transplantation. Thus, ischemia/reperfusion (I/R) injury is a biphasic phenomenon that can damage the graft by inflammatory responses. The hypothalamic-pituitary-adrenal (HPA) axis is the main hormonal system that is activated under the influence of stress. Normal HPA axis activity leading to the release of glucocorticoids is essential for homeostasis and survival during stress. Cortisol, a key controller of stress response, is released by the HPA axis. The disrupted release of cortisol in response to inflammation has been shown in animal models. Nesfatin-1 is a peptide involved in the regulation of homeostasis and has anti-inflammatory as well as anti-ischemic properties. Therefore, we aimed to identify the effect of chronic peripheral nesfatin-1 application on the plasma level of cortisol in a rat model of intestinal I/R-based stress. Materials and Methods: Two-month-old 28 Wistar Albino male rats that weighed an average of 200-250 g were used and were randomly divided into the following four experimental groups (n=7): laparotomy, I/R, nesfatin-1+laparotomy, nesfatin-1+I/R. Blood samples were collected in tubes with EDTA. Plasma cortisol levels were analyzed by rat enzyme-linked immunosorbent assay (ELISA) kits.Results: Statistically significant decrease was found in the plasma level of cortisol in nesfatin-1+I/R group compared with I/R group (p=0.026) Conclusion: Nesfatin-1 application can inhibit anti-inflammatory responses under the early phase of intestinal I/R and support immune reactions by reducing plasma cortisol level. This effect of nesfatin-1 may also increase the rejection of grafts during transplantation period

🔖

Cite This Article

TORU, Ü., AYADA, C., GENÇ, O., AKCILAR, R., ŞAHİN, S., ERKEN, G., ERKEN, H. A., TURGUT, G., TURGUT, S. (2015). Possible Activation of the Immune System by Chronic Peripheral Nesfatin-1 Application at the Acute Phase of Ischemia/Reperfusion Injury. Erciyes Medical Journal, Cilt: 37 - Sayı: 4, 143–147. https://ajindex.com/articles/207710

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (3)

  1. Romero ML, Butler Luke K. Endocrinology of Stress. Int J Comp Psychol 2007; 20: 89-95. Gambarana C. Experimental protocols for the study of stress in ani- mals and humans. Nutrients, stress and medical disorders. (Eds) Ye- huda S and Mostofsky D Human press Inc Totowa 2005; 21-30.
  2. Matteri RL, Carroll JA, Dyer CJ. Neuroendocrine responses to stress. In: Moberg GP, Mench JA, editors. The Biology of animal stress. CABI Publishing; 2000. p. 43-76. [CrossRef] Uchoa ET, Aguilera G, Herman JP, Fiedler JL, Deak T, de Sousa MB. Novel aspects of glucocorticoid actions. J Neuroendocrinol 2014; 26(9): 557-72. [CrossRef] Gill R, Tsung A, Billiar T. Linking oxidative stress to inflammation: Toll-like receptors. Free Radic Biol Med 2010; 48(9): 1121-32. [CrossRef] Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury. J Pathol 2000; 190(3): 255-66. [CrossRef] Otukesh H, Hoseini R, Rahimzadeh N, Hosseini S, Ahmadpoor P, Ja- vadi Larijani F. The role of Ischemia reperfusion damage on renal trans- plant, what are the new treatments? J Ped Nephrology 2013; 1: 1-7.
  3. Gottlieb RA, Mentzer RM. Autophagy during cardiac stress: joys and frustrations of autophagy. Annu Rev Physiol 2010; 72: 45-59. [CrossRef] Rhen T, Cidlowski JA. Antiinflammatory action of glucocorticoids--new mechanisms for old drugs. N Engl J Med 2005; 353(16): 1711-23. [CrossRef] Chrousos GP, Gold PW. A healthy body in a healthy mind--and vice versa--the damaging power of "uncontrollable" stress. J Clin Endocri- nol Metab 1998; 83(6): 1842-5. [CrossRef] Ulrich-Lai YM, Herman JP. Neural regulation of endocrine and au- tonomic stress responses. Nat Rev Neurosci 2009; 10(6): 397-409. [CrossRef] Rae MT, Hillier SG. Steroid signalling in the ovarian surface epithe- lium. Trends Endocrinol Metab 2005; 16(7): 327-33. [CrossRef] Oh-I S, Shimizu H, Satoh T, Okada S, Adachi S, Inoue K, et al. Iden- tification of nesfatin-1 as a satiety molecule in the hypothalamus. Na- ture 2006; 443(7112): 709-12. [CrossRef] Shimizu H, Oh-I S, Okada S, Mori M. Nesfatin-1: an overview and future clinical application. Endocr J 2009; 56(4): 537-43. [CrossRef] Gunay H, Tutuncu R, Aydin S, Dag E, Abasli D. Decreased plasma nesfatin-1 levels in patients with generalized anxiety disorder. Psycho- neuroendocrinology 2012; 37(12): 1949-53. [CrossRef] Angelone T, Filice E, Pasqua T, Amodio N, Galluccio M, Montesanti G, et al. Nesfatin-1 as a novel cardiac peptide: identification, func- tional characterization, and protection agains