2Department of Physiology, Dumlupınar University Faculty of Medicine, Kütahya, Turkey
3Department of Medical Biology, Dumlupınar University Faculty of Medicine, Kütahya, Turkey
4Department of Physiology, Balıkesir University Faculty of Medicine, Balıkesir, Turkey
5Department of Physiology, Pamukkale University Faculty of Medicine, Denizli, Turkey
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.[¤]