[Protective effects of the flavonoids osajin and pomiferin on heart ischemia-reperfusion]. / Protektivní efekt flavonoidu osajinu a pomiferinu na ischémii-reperfuzi srdce.

The study was undertaken to evaluate the cardioprotective potential of the flavonoids osajin and pomiferin against ischemia-reperfusion induced injury in rat hearts as a model of antioxidant-based composite therapy. Studies were performed with isolated, modified Langendorff-perfused rat hearts and ischemia of the heart was initiated by stopping the coronary flow for 30 min followed by 60 min of reperfusion (14 ml x min(-1)). Wistar rats were divided into four groups. The treated groups received osajin or pomiferin (5 mg/kg/day in 0.5% Avicel), the placebo group received only 0.5 Avicel; the intact group was left without any applications. Biochemical indicators of oxidative damage--malondialdehyde, superoxide dismutase, glutathione peroxidase, total antioxidant activity in serum and the myocardium have been evaluated. We also examined the effect of osajin and pomiferin on cardiac function: left ventricular end-diastolic pressure, left ventricular pressure, and peak positive dP/dt. Our results demonstrate that the flavonoids osajin and pomiferin attenuate the myocardial dysfunction provoked by ischemia-reperfusion. This was confirmed by an increase in both the antioxidant enzyme values and the total antioxidant activity. The cardioprotection provided by osajin and pomiferin treatment results from the suppression of oxidative stress and correlates with the improved ventricular function.

Protective effects of osajin in ischemia-reperfusion of laboratory rat kidney.

The aim of this study was to analyze the antioxidative effect of osajin during prophylactic administration. The pathological model for in vivo experiment was the unilateral ischemia-reperfusion of kidney of the laboratory rat. The animals were randomly divided into five groups. Osajin was administrated orally in doses of 5, 10 and 20 mg/kg once a day to three premedicated groups. Placebo--0.5% solution of Avicel--was given to the fourth group and the fifth group was completely intact. The premedication lasted 15 days and subsequently the ischemia of the left kidney was incited in general anaesthesia for 60 min. The reperfusion lasted 10 min and it was finished by blood collection from the left ventricle and the reperfused kidney was recovered. Selected biochemical markers were assessed in blood: superoxide dismutase, glutathion peroxidase, total antioxidative capacity and malondialdehyde. The kidney tissue samples were used for histopathological examination. Laboratory and histopathological results confirmed supposed effects of osajine. The dependence between the effect and the applied dose of osajin was linear. The best biochemical results were reached after administration of osajin at the dose of 5 mg/kg. The best histopathological results were reached after administration of osajin at the dose of 10 mg/kg.

[Morin in the therapy of the ischemia-reperfusion damage model of the rat kidney]. / Morin v terapii ischemicko-reperfuzního poskození ledvinné tkáne laboratorního potkana.

The aim of this study was to analyze the protective effects of morin administered during the therapy of reperfusion injury of the laboratory rat kidney. Animals were randomly divided into five groups (n= 10). One group was left intact. Three medicated groups and one placebo group were subjected to ischemia (60 min) and reperfusion of the left kidney. Morin was suspended in a 2 ml of 0.5% Avicel solution and administered orally by a gastric probe at doses of 5, 10, and 20 mg.kg(-1) once a day for 15 days. The placebo group was given only 2 ml of 0.5% Avicel in the same way. On the 15th day, all the animals were exsanguinated and the reperfused kidneys were recovered. Selected biochemical markers in blood were assessed: superoxide dismutase, glutathion peroxidase, total antioxidative capacity, malondialdehyde, creatinine, urea, and uric acid. Creatinine, urea, and total protein were analyzed in urine, and a 24-hour diuresis was recorded. The kidney tissue samples were used for histopathological examination. Morin supported the organism's own defensive reactions against free radicals and decreased lipid peroxidation in the cell membranes and contributed to the recovery of kidney functions. The histopathological results confirm 20 mg x kg(-1) as the most effective dose.

[Prophylactic administration of homoisoflavonoid in ischemic-reperfusion damage of the renal tissue in the laboratory rat]. / Profylaktické podávání homoizoflavonoidu u ischemicko- reperfuzního poskození ledvinné tkáne laboratorního potkana.

The study aimed to examine the antioxidizing effect of homoisoflavonoid in prophylactic administration under the conditions of renal ischemia-reperfusion in the laboratory rat. The pathological model for the in vivo experiment was unilateral renal ischemia-reperfusion of the laboratory rat. The animals were randomized into 5 groups. Homoisoflavonoid was administered to treated groups orally in doses of 5, 10 and 20 mg/kg once a day in 0.5% Avicel solution. The placebo group received Avicel only, and the intact group was without medication and intervention. On day 15 of the experiment, renal tissue ischemia/reperfusion (60/10 mins) was induced in the treated and placebo groups. Then the animals were exsanguinated, biochemical parameters in the blood (superoxidismutase, glutathionperoxidase, total antioxidizing capacity and malondialdehyde) were assayed, and renal samples were withdrawn for histopathological examination. A biochemical examination demonstrated a dependence of the effect of homoisoflavonoid on the dose administered. An obvious effect was demonstrated in the values of GSHPx, AOC, and MDA. On the other hand, a negative dependence was found between the dose of administered homoisoflavonoid and SOD and GSHPx values. The results of biochemical examination correlate with the histopathological pictures of the renal tissue and support the assumption about a protective effect of homoisoflavonoid under the conditions of artificially induced pathological state--renal tissue ischemia-reperfusion.