BACKGROUND: Mesna is a thiol used for the prevention of oxazaphosphorine-induced hemorrhagic cystitis. However, its antioxidant properties on renal and hepatorenal oxidative damage, as well as its mucoprotective effect on the intestinal epithelium have also been shown. The aim of this study was to investigate the potential beneficial effect of mesna on ischemia/reperfusion (I/R)-induced oxidant damage of the intestinal mucosa. MATERIALS AND METHODS: Wistar rats were subjected to intestinal I/R for 30 min, induced by occlusion of the superior mesenteric artery, followed by 60 min reperfusion. Mesna was administered at 3 time points relative to ischemia; 60 min before ischemia, at the onset of ischemia or at the onset of reperfusion. At the end of the study period, jejunal segments were excised and assessed for histopathologic score, apoptotic index using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) assay and glutathione/glutathione disulfide (GSH/GSSG) ratio, as a marker of oxidative stress. RESULTS: I/R caused deterioration of histological characteristics and induction of apoptosis and oxidative stress in the intestinal mucosa. Changes regarding histology and apoptosis were prevented when mesna was administered 60 min before ischemia, but were attenuated when mesna was administered at the onset of ischemia or reperfusion. In all mesna groups, oxidative stress was reduced. CONCLUSIONS: Mesna can ameliorate or even prevent intestinal I/R injury by reducing oxidative stress.
BACKGROUND:Mesna is a thiol used for the prevention of oxazaphosphorine-induced hemorrhagic cystitis. However, its antioxidant properties on renal and hepatorenal oxidative damage, as well as its mucoprotective effect on the intestinal epithelium have also been shown. The aim of this study was to investigate the potential beneficial effect of mesna on ischemia/reperfusion (I/R)-induced oxidant damage of the intestinal mucosa. MATERIALS AND METHODS:Wistar rats were subjected to intestinal I/R for 30 min, induced by occlusion of the superior mesenteric artery, followed by 60 min reperfusion. Mesna was administered at 3 time points relative to ischemia; 60 min before ischemia, at the onset of ischemia or at the onset of reperfusion. At the end of the study period, jejunal segments were excised and assessed for histopathologic score, apoptotic index using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) assay and glutathione/glutathione disulfide (GSH/GSSG) ratio, as a marker of oxidative stress. RESULTS: I/R caused deterioration of histological characteristics and induction of apoptosis and oxidative stress in the intestinal mucosa. Changes regarding histology and apoptosis were prevented when mesna was administered 60 min before ischemia, but were attenuated when mesna was administered at the onset of ischemia or reperfusion. In all mesna groups, oxidative stress was reduced. CONCLUSIONS:Mesna can ameliorate or even prevent intestinal I/R injury by reducing oxidative stress.
Authors: Samia Adel Abd El-Baset; Manal R Abd El-Haleem; Rehab S Abdul-Maksoud; Asmaa A A Kattaia Journal: Sci Rep Date: 2021-06-25 Impact factor: 4.379