Abstract
BACKGROUND: Ischemia-reperfusion (I-R) injury associated with acute mesenteric vascular occlusion can lead to severe impairment of intestinal tissue and may become a life-threatening condition if not treated in the early clinical stages. Previous studies have suggested that fraxin may exert protective effects against I-R-induced mesenteric injury due to its antioxidant and anti-inflammatory properties. METHODS: This experimental study was conducted using healthy male Wistar albino rats. The animals were divided into four groups: a Sham group (superior mesenteric artery [SMA] isolated but not occluded), a Control group (SMA isolated and I-R induced), a 10 mg/kg Fraxin group, and a 50 mg/kg Fraxin group (fraxin administered before reperfusion). Total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities were evaluated. Histopathological examinations and inflammatory markers, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and myeloperoxidase (MPO), were also analyzed. RESULTS: In the Sham group, SOD activity was 135.2±10.5 U/mg protein, GPx activity was 65.3±4.7 U/mg protein, and CAT activity was 85.1±5.8 U/mg protein. In the Control group, these values were 95.4±7.9, 45.7±3.6, and 60.3±4.2 U/mg protein, respectively. In 10 mg/kg Fraxin group, SOD, GPx, and CAT activities were 115.6±8.4, 55.8±4.2, and 75.6±5.5 U/mg protein, respectively; in the 50 mg/kg Fraxin group, the corresponding values were 130.8±9.7, 60.2±4.8, and 90.4±6.3 U/mg protein. Significant decreases in TNF-α, IL-6, and MPO levels were observed in the Fraxin-treated groups (p<0.05). CONCLUSION: Fraxin administration preserved tissues and improved antioxidant parameters by reducing oxidative stress and inflammation in the acute mesenteric artery ischemia-reperfusion injury (AMAIRI) model. Based on these findings, fraxin may be considered a potential therapeutic option for mesenteric ischemia-reperfusion-related injuries.