Abstract
To investigate the potential protective effects of erdosteine against the harmful effects of ischemia-reperfusion injury on the liver in an experimental rat model. Forty rats were divided into 4 groups. In the sham group, only the hepatic pedicle was mobilized. No other manipulation or treatment was performed. In the other groups, ischemia was achieved by clamping the hepatic pedicle for 60 min. After that, 90 min reperfusion was provided. In the control group, no treatment was given. In the perioperative treatment group, 100 mg/kg erdosteine was administered 2 hours before ischemia induction. In the preoperative treatment group, 100 mg/kg/day erdosteine was administered daily for ten days before the operation. At the end of the procedures, blood and liver samples were obtained for biochemical and histopathological assessment. Treatment with erdosteine ameliorated the histopathological abnormalities when compared with the control group. Furthermore, this treatment significantly decreased the serum liver function test values. It was also found that erdosteine ameliorated the oxidative stress parameters in both the perioperative and preoperative treatment groups. The current study is the first to have shown the favorable effects of erdosteine on the harmful effects of experimental hepatic ischemia-reperfusion injury.
Highlights
Ischemia-reperfusion injury (IRI) is an inevitable situation in a wide range of surgical settings and has an important impact on the clinical outcome
The use of preoperative and perioperative erdosteine decreased these levels significantly when compared with the control group (p
The results of the present study showed that erdosteine ameliorated the harmful effects of ischemia-reperfusion injury on the liver
Summary
Ischemia-reperfusion injury (IRI) is an inevitable situation in a wide range of surgical settings and has an important impact on the clinical outcome. It occurs when the blood supply is interrupted for a prolonged period of time and is restored. Tissues are deprived of oxygen and nutrients, leading to cellular metabolism breakdown. After blood flow restoration (reperfusion), more severe damage is provoked in the ischemic tissue due to the production of reactive oxygen species (ROS), progressing to extended inflammation and necrotic and apoptotic events which result in organ injury[1]. Promising agents and strategies against IRI have not yet become part of the clinical routine[2]
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