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J Jurica

Publications and source records attributed to J Jurica.

6 recordsLinked to original sources
PubMed2006

[Morin in the therapy of the ischemia-reperfusion damage model of the rat kidney].

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.

Animals↗
PubMed2006

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.

Animals↗
PubMed2005

Effect of St John's wort (Hypericum perforatum) on cytochrome P-450 activity in perfused rat liver.

St. John's wort (Hypericum perforatum) is a popular over-the-counter dietary supplement and a herbal antidepressant that has been implicated in drug interactions with substrates of several cytochrome P-450 (CYP) isozymes. The effects of the St. John's wort extract (100 mg/kg, i.p., once daily for 10 days) on metabolic activity of CYP450 were assessed in the system of isolated perfused rat liver. The substrates used in this study were tolbutamide (CYP2C6), dextromethorphan (CYP2D2) and midazolam (CYP3A2). Validated HPLC method was used to quantify all compounds of interest. St. John's wort administration affected CYP activity, causing a significant decline in AUC of dextromethorphan [F(4,31)=1511, p<0.001; PLSD, p<0.001] and AUC of midazolam [F(3,25)=221, p<0.001; PLSD, p=0.035] and a significant increase in AUC of tolbutamide [F(3,26)=200, p<0.001; PLSD, p<0.001]. St. John's wort administration resulted in a significant induction of CYP2D2 and CYP3A2, and in a significant inhibition of CYP2C6 metabolic activities.

Animals↗
PubMedDate not supplied

Effect of methamphetamine on the pharmacokinetics of dextromethorphan and midazolam in rats.

Methamphetamine is the fourth most frequently reported compound associated with drug abuse on admission of patients to treatment centres after cocaine, heroin and marijuana. It is metabolized in the organism with a reaction that is catalyzed by cytochrome P450, mainly by the CYP2D and CYP3A subfamily, 4-hydroxyamphetamine and amphetamine being dominant metabolites. The present pharmacokinetic study was undertaken to investigate the possible influence of methamphetamine (10 mg/kg, i.p., once daily for six days) on the pharmacokinetics of dextromethorphane as a model substrate for rat cytochrome P-4502D2 and midazolam as a model substrate for CYP3A1/2. Animals received a single injection of dextromethorphane (10 mg/kg) or midazolam (5 mg/kg) in the tail vein 24 h after the last dose of methamphetamine or administration of placebo. The results of pharmacokinetic analysis showed a significantly increased rate of dextrorphane and 3-hydroxymorphinan formation, and a marked stimulatory effect of methamphetamine on CYP2D2 metabolic activity. Similarly, the kinetics of midazolam's metabolic conversion to hydroxy derivates of midazolam indicated a significant increase in CYP3A1/2 activity. The results showed that the administration of methamphetamine significantly stimulated the metabolic activity of CYP2D2 as well as that of CYP3A1/2. With regard to the high level of homology between human and rat CYP isoforms studied, the results may have a clinical impact on future pharmacotherapy for methamphetamine abuse.

Alcohol Oxidoreductases↗