Abstract
To investigate the effect of metyrosine against I/R induced gastric damage in rats. Eighteen albino Wistar male rats were divided into groups; gastric I/R (GIR), 50 mg/kg metyrosine+gastric I/R (MGIR), and sham (SG) groups. 50 mg/kg metyrosine was given to the MGIR group, and distilled water was given to the GIR and SG groups by the oral gavage. After 30 minutes, 25 mg/kg thiopental sodium was injected intraperitoneally. Ischemia was achieved for 1 hour by clamping the celiac artery of the MGIR and GIR groups, then reperfusion was achieved for 3 hours. After that, animals were killed with 50 mg/kg thiopental. Biochemical and histopathological examinations performed on the gastric tissues. Metyrosine decreased the MDA and MPO and the increased the tGSH and SOD. In addition, it reduced inflammation by suppressing the decrease of COX-1 and the increase of COX-2. Histopathologically, metyrosine decreased symptoms caused by I/R such as mucosal necrosis, hemorrhage, edema, PMNL infiltration, and dilated congested blood vessels. Metyrosine prevented the I/R induced oxidative stress in the gastric tissue. Metyrosine may be beneficial for gastric I/R injury.
Highlights
Gastric ischemia/reperfusion (I/R) injury can occur during a variety of surgical procedures and due to a number of pathological conditions such as vascular rupture, gastrointestinal disease, and hemorrhagic shock[1]
Excessive free oxygen radicals (FOR) forming from the molecular oxygen abundantly introduced by arterial blood to the ischemic tissue during reperfusion is held responsible for reperfusion injury[3]
While there is no statistical difference between the metyrosine group and the healthy group, there is a significant difference between the metyrosine and I/R groups (p
Summary
Gastric ischemia/reperfusion (I/R) injury can occur during a variety of surgical procedures and due to a number of pathological conditions such as vascular rupture, gastrointestinal disease, and hemorrhagic shock[1]. Excessive free oxygen radicals (FOR) forming from the molecular oxygen abundantly introduced by arterial blood to the ischemic tissue during reperfusion is held responsible for reperfusion injury[3]. These increased FORs can lead to tissue lipid peroxidation, causing cellular death and mucosal damage[4]. None of the natural antioxidant systems have the ability to protect against the attack of oxidants induced by I/R7,8. For this reason, antioxidant and antiinflammatory agents have been tried and found effective against gastric I/R injury[9]. There are studies reporting the antioxidant activity of metyrosine[11]
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