Abstract
The aim of the study was to analyse protective effects of different doses of pomiferin in therapy of reperfusion injury. Rats were randomly divided into five groups (n=10). One group was intact. Three medicated groups and one placebo group were subjected to ischaemia and reperfusion of the left kidney. Pomiferin was administrated by single gastric gavage in 2 ml of 0.5% Avicel solution in doses of 5, 10 and 20 mg/kg. The placebo group was given only Avicel solution. On day 15, all the animals were exsanguinated and the reperfused kidneys were recovered. Selected biochemical markers were assessed in blood: antioxidative enzymes, total antioxidative capacity, malondialdehyde, creatinine, urea and uric acid. Creatinine, urea and total proteins were analysed in urine and 24-hour diuresis was recorded. The kidney tissue samples were used for histopathological examination.The results confirmed the expected protective effects of pomiferin. Pomiferin supported defensive reactions of the body against free radicals (increased levels of superoxide dismutase, total antioxidative capacity), decreased lipid peroxidation (decreased malondialdehyde) and contributed to the recovery of kidney functions (creatinine and urea in blood). The best biochemical and histopathological results were achieved after pomiferin administration in the dose of 5 mg/kg.
Highlights
Reactive oxygen or nitrogen species (ROS/RNS) are constantly formed in the organism during physiological processes or they are derived from external sources and eliminated by the antioxidant defence of the organism (Yu, 1994)
The aim of the study was to analyse the effects of different doses of pomiferin administered during the therapy of ischaemia-reperfusion injury of kidney tissue in laboratory rats
In the 1st tissue structure the best result was achieved after administration of the highest dose of pomiferin – 20 mg/kg, the average score of this tissue structure being 1.0
Summary
Reactive oxygen or nitrogen species (ROS/RNS) are constantly formed in the organism during physiological processes or they are derived from external sources and eliminated by the antioxidant defence of the organism (Yu, 1994). A balance exists between the level of ROS and the level of endogenous antioxidants. When this balance is disrupted, oxidative stress occurs. In reperfusion – reoxygenation of ischaemic tissue – XOD becomes the main source of ROS. Production of ROS is very fast – in the ischaemic myocardium ROS are detected in the first minutes after reperfusion (Zhao, 2004). ROS attack cells, induce synthesis of adhesive molecules which attract neutrophils – producers of other ROS molecules (Drabikova et al, 2002).
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