The effects of sulforaphane in the rat model of experimental intestinal ischemia reperfusion

Abstract

Aim The aim of this study is to investigate the effects of sulforaphane (SFN), which has been shown to protect such organs as the brain, kidneys, liver, and heart against the injury caused by ischemia reperfusion (I-R), on the reperfusion injury in the experimental intestinal I-R model.Material and method The study employed 30 Wistar albino rats, and there were three groups: the control group (n = 10), I-R group (n = 10), and SFN + I-R group (n = 10). The rats in the control group were sacrificed after a 3-h follow-up subsequent to the laparotomy. The I-R group was subjected to an hour of ischemia and 2 h of reperfusion afterward. The SFN + I-R group was administered a dose of 3 mg/kg SFN intraperitoneally. The rats were sacrificed after the ileum resection for measurement of tissue malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activity and histopathological analysis.Results The I-R and SFN + I-R groups were histopathologically shown to have similar cell injuries. In the SFN + I-R group, the increase in GSH-Px activity was higher than SOD activity and both of the increases were statistically significant compared with the control group (p < 0.001). The SFN application did not yield a significant difference in the tissue MDA level compared with the control group.Conclusion The effect of SFN use on the I-R injury in the intestine did not show an apparent effect histopathologically, although there were statistically significant differences in biochemical parameters.

Effects of bradykinin preconditioning in an experimental intestinal ischemia reperfusion model on rats

“…Histopathological changes in the jejunum due to IR injury were evaluated according to the grading of Chiu et al 3…”

“…The pathogenesis of ischemia reperfusion (IR) is due to both the depletion of cellular energy sources due to tissue hypoxia during ischemia and, more importantly, to the formation of O2-derived free radicals during reperfusion. The IR process can cause dysfunction and damage not only to the organ in which it is involved but also to distant organs through a range of mediators 3 .…”