Balanced oxidative status by nesfatin-1 in intestinal ischemia-reperfusion

Abstract

Objective: Ischemia causes reversible or irreversible cell or tissue damage and reperfusion can exaggerate cellular damage. Microvascular dysfunction is induced and causes enhanced fluid filtration in capillaries. At the acute phase of reperfusion more oxygen radicals are activated. Nesfatin-1 protects brain against oxidative damage and heart against ischemia/reperfusion damage. In our study, we aimed to investigate the acute effect of chronic peripheral nesfatin-1 administration in intestinal ischemia/reperfusion created rats.

Method: Two-months-old, 28 Wistar Albino male rats, weighing an average of 200-250 g, were used and randomly divided into four experimental groups (n=7) as; Laparotomy, Ischemia/Reperfusion, Nesfatin-1+Laparotomy, Nesfatin-1+Ischemia/Reperfusion. Serum levels of total oxidant status (TOS) and total antioxidant status (TAS) were determined by colorimetric measurement method. The plasma levels of endotelin-1 and endothelial nitric oxide syntheses (eNOS) were analyzed by rat ELISA assay kits.

Results: Plasma levels of endothelin-1 significantly increased, plasma level of eNOS, serum levels of TOS and TAS significantly decreased in nesfatin-1 applied groups. Additionally, The oxidative stress index (OSI) parameters decreased significantly in three groups compared to laparotomy.

Conclusion: Chronic peripheral nesfatin-1 administration can decrease eNOS level and OSI at the acute phase of ischemia/reperfusion. We suppose that it can be protective for ischemia/reperfusion injury by balancing oxidant capacity. On the other hand, this effect of nesfatin-1 is not related with micro-circular compensation and increases anti-oxidant capacity.

Keywords: Nesfatin-1; eNOS; endothelin-1; ischemia/reperfusion; total antioxidant capacity; total oxidant capacity.

Figure 1

Plasma levels of endothelin-1 in L, I/R, N+L and N+I/R groups. †: The significance between L and the other groups, P<0.05 (Mann Whitney U test). **: The significance between L and the other groups, P<0.01 (Mann Whitney U test). ##: The significance between I/R and the other groups, P<0.01 (Mann Whitney U test).

Figure 2

Plasma levels of eNOS in L, I/R, N+L and N+I/R groups. **: The significance between L and the other groups, P<0.01 (Mann Whitney U test). #: The significance between I/R and the other groups, P<0.05 (Mann Whitney U test).

Figure 3

Serum levels of TOS in in L, I/R, N+L and N+I/R groups. **: The significance between L and the other groups, P<0.01 (Mann Whitney U test). ##: The significance between I/R and the other groups, P<0.01 (Mann Whitney U test).

Figure 4

Serum levels of TAS in L, I/R, N+L and N+I/R groups. *,#: The significance between L and the other groups, P<0.05 (Mann Whitney U test). ††: The significance between L and the other groups, P<0.01 (Mann Whitney U test). ¶¶, aa: The significance between I/R and the other groups, P<0.01 (Mann Whitney U test).

Figure 5

The oxidative stress index (OSI) of L, I/R, N+L and N+I/R groups. *, †: The significance between L and the other groups, P<0.05 (Mann Whitney U test). ##: The significance between L and the other groups, P<0.01 (Mann Whitney U test).

Figure 6

Suggested mechanism for the action of nesfatin-1 on the balanced oxidative status induced by ischemia/reperfusion. eNOS; endothelial nitric oxide syntheses, MnSOD; Manganese superoxide dismutase, GPs; Gypenosides, ONOO^-; Peroxynitrite, ROS; Reactive oxygen species, RNS; Reactive nitrogen species.