Elżbieta Wyska
Jagiellonian University Medical College
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Featured researches published by Elżbieta Wyska.
Pharmacology, Biochemistry and Behavior | 2014
Kinga Sałat; Agnieszka Cios; Elżbieta Wyska; Robert Sałat; Szczepan Mogilski; Barbara Filipek; Krzysztof Więckowski; Barbara Malawska
BACKGROUND Anticancer drugs - oxaliplatin (OXPT) and paclitaxel (PACLI) cause painful peripheral neuropathy activating Transient Receptor Potential (TRP) channels. Here we investigated the influence of 3-[4-(3-trifluoromethyl-phenyl)-piperazin-1-yl]-dihydrofuran-2-one (LPP1) and pregabalin on nociceptive thresholds in neuropathic pain models elicited by these drugs. Pharmacokinetics of LPP1 and its ability to attenuate neurogenic pain caused by TRP agonists: capsaicin and allyl isothiocyanate (AITC) were also investigated. METHODS Antiallodynic and antihyperalgesic effects of intraperitoneally administered LPP1 and pregabalin were tested in the von Frey, hot plate and cold water tests. The influence of LPP1 on locomotor activity and motor coordination was assessed using actimeters and rotarod. Serum and tissue concentrations of LPP1 were measured using the HPLC method with fluorimetric detection. RESULTS In OXPT-treated mice LPP1 and pregabalin dose-dependently reduced tactile allodynia (41-106% and 6-122%, respectively, p<0.01). At the dose of 10mg/kg LPP1 attenuated cold allodynia. In PACLI-treated mice LPP1 and pregabalin reduced tactile allodynia by 12-63% and 8-50%, respectively (p<0.01). Both drugs did not affect cold allodynia, whereas pregabalin (30 mg/kg) attenuated heat hyperalgesia (80% vs. baseline latency time; p<0.01). No motor impairments were observed in LPP1 or pregabalin-treated neuropathic mice in the rotarod test, while severe sedation was noted in the locomotor activity test. LPP1 reduced pain induced by capsaicin (51%; p<0.01) and AITC (41%; p<0.05). The mean serum concentration of LPP1 measured 30 min following i.p. administration was 7904.6 ± 1066.1 ng/ml. Similar levels were attained in muscles, whereas brain concentrations were 62% lower. Relatively high concentrations of LPP1 were also determined in the cerebrospinal fluid and the sciatic nerve. CONCLUSIONS LPP1 and pregabalin reduce pain in OXPT and PACLI-treated mice. This activity of LPP1 might be in part attributed to the inhibition of TRPV1 and TRPA1 channels, but also central mechanisms of action cannot be ruled out.
Experimental Gerontology | 2014
Agnieszka Cios; Elżbieta Wyska; Joanna Szymura-Oleksiak; Tomasz Grodzicki
The aims of the study were to develop a population pharmacokinetic model of ciprofloxacin (CPX) in the elderly patients and to examine the impact of patient-dependent variables on pharmacokinetic parameter values of this drug. The study was conducted in a group of 44 patients at the age of 44-96years, hospitalized due to pneumonia lobaris or bronchopneumonia. Patients received CPX at a dose of 200mg every 12h as a constant rate infusion over 0.5h. Concentrations of CPX in serum were measured by HPLC with UV detection. Population pharmacokinetic analysis revealed that CPX concentration versus time data were best described by a one-compartment model. The mean values of volume of distribution and clearance of CPX in the patients above 65years of age were 78.41±13.17L and 18.39±4.15L/h, respectively. The creatinine clearance influenced CPX clearance according to the equation: CLCPX (L/h)=8.0+0.21·CLCr, while the volume of distribution of CPX was dependent on the body weight of the patient as follows: VdCPX (L)=22.72+0.86·WT. In summary, the developed population model can be used to assess the pharmacokinetic parameters of CPX in the elderly patients and to select on the basis of these parameters and MIC values an optimal dosage regimen of this drug.
Toxicology and Applied Pharmacology | 2017
Katarzyna Socała; Dorota Nieoczym; Edyta Kowalczuk-Vasilev; Elżbieta Wyska; Piotr Wlaź
ABSTRACT Activation of Nrf2 with sulforaphane has recently gained attention as a new therapeutic approach in the treatment of many diseases, including epilepsy. As a plant‐derived compound, sulforaphane is considered to be safe and well‐tolerated. It is widely consumed, also by patients suffering from seizure and taking antiepileptic drugs, but no toxicity profile of sulforaphane exists. Since many natural remedies and dietary supplements may increase seizure risk and potentially interact with antiepileptic drugs, the aim of our study was to investigate the acute effects of sulforaphane on seizure thresholds and activity of some first‐ and second‐generation antiepileptic drugs in mice. In addition, some preliminary toxicity profile of sulforaphane in mice after intraperitoneal injection was evaluated. The LD50 value of sulforaphane in mice was estimated at 212.67 mg/kg, while the TD50 value – at 191.58 mg/kg. In seizure tests, sulforaphane at the highest dose tested (200 mg/kg) significantly decreased the thresholds for the onset of the first myoclonic twitch and generalized clonic seizure in the iv PTZ test as well as the threshold for the 6 Hz‐induced psychomotor seizure. At doses of 10–200 mg/kg, sulforaphane did not affect the threshold for the iv PTZ‐induced forelimb tonus or the threshold for maximal electroshock‐induced hindlimb tonus. Interestingly, sulforaphane (at 100 mg/kg) potentiated the anticonvulsant efficacy of carbamazepine in the maximal electroshock seizure test. This interaction could have been pharmacokinetic in nature, as sulforaphane increased concentrations of carbamazepine in both serum and brain tissue. The toxicity study showed that high doses of sulforaphane produced marked sedation (at 150–300 mg/kg), hypothermia (at 150–300 mg/kg), impairment of motor coordination (at 200–300 mg/kg), decrease in skeletal muscle strength (at 250–300 mg/kg), and deaths (at 200–300 mg/kg). Moreover, blood analysis showed leucopenia in mice injected with sulforaphane at 200 mg/kg. In conclusion, since sulforaphane was proconvulsant at a toxic dose, the safety profile and the risk‐to‐benefit ratio of sulforaphane usage in epileptic patients should be further evaluated. HIGHLIGHTSSulforaphane, an Nrf2 activator, is proconvulsant at toxic doses in mice.Sulforaphane at 100 mg/kg produces a pharmacokinetic interaction with carbamazepine.Sulforaphane has an LD50 of 212.67 mg/kg in mice (after ip administration).The risk‐to‐benefit ratio of sulforaphane needs further evaluation.
Toxicology and Applied Pharmacology | 2017
Aleksandra Szopa; Urszula Doboszewska; Mariola Herbet; Sylwia Wośko; Elżbieta Wyska; Katarzyna Świąder; Anna Serefko; Agnieszka Korga; Aleksandra Wlaź; Andrzej Wróbel; Marta Ostrowska; Joanna Terlecka; Adam Kanadys; Ewa Poleszak; Jarosław Dudka; Piotr Wlaź
&NA; Recent preclinical and clinical data suggest that low dose of caffeine enhances the effects of common antidepressants. Here we investigated the effects of chronic administration of caffeine (5 mg/kg, twice daily for 14 days) and its withdrawal on day 15th on the activity of per se ineffective doses of fluoxetine (5 mg/kg) and escitalopram (2 mg/kg) given on day 15th. We found decreased immobility time in the forced swim and tail suspension tests in mice in which caffeine was administered simultaneously with antidepressants on day 15th following a 14‐day caffeine treatment and no alterations in the spontaneous locomotor activity. A decrease in the level of escitalopram and an increase in the level of caffeine in serum were observed after concomitant administration of these compounds, while the joint administration of caffeine and fluoxetine was not associated with changes in their levels in serum or brain. Caffeine withdrawal caused a decrease in Adora1 mRNA level in the cerebral cortex (Cx). Administration of escitalopram or fluoxetine followed by caffeine withdrawal caused an increase in this gene expression, whereas administration of escitalopram, but not fluoxetine, on day 15th together with caffeine caused a decrease in Adora1 mRNA level in the Cx. Furthermore, antidepressant‐like activity observed after joint administration of the tested drugs with caffeine was associated with decreased Slc6a15 mRNA level in the Cx. The results show that withdrawal of caffeine after its chronic intake may change activity of antidepressants with concomitant alterations within monoamine, adenosine and glutamate systems. HighlightsCaffeine was administered for 14 days and on day 15th it was withdrawn.Ineffective doses of fluoxetine or escitalopram (FLX/ESC) were administered on day 15th.FLX/ESC given together with caffeine displayed antidepressant‐like activity.Caffeine and FLX/ESC modified Adora1 and Slc6a15 mRNA level in the cerebral cortex.Caffeine withdrawal after its chronic intake may change activity of FLX/ESC.
Xenobiotica | 2015
Malgorzata Szafarz; Agata Kryczyk; Dorota Lażewska; Katarzyna Kieć-Kononowicz; Elżbieta Wyska
Abstract 1. The aim of this study was to evaluate pharmacokinetics and tissue distribution of novel histamine H3 receptor antagonist 1-[3-(4-tert-butylphenoxy)propyl]piperidine (compound DL76). 2. Following intravenous administration of DL76 at the dose of 3 mg/kg, pharmacokinetic parameters were calculated using non-compartmental analysis. The systemic serum clearance was 10.08 L/h/kg and the estimated blood clearance was 5.64 L/h/kg. The volume of distribution at steady state was 16.1 L/kg which was greater than total body water, terminal half-life and MRT equalled 1.41 h and 1.6 h, respectively. The two-compartment pharmacokinetic model with enterohepatic circulation was also successfully fitted to the experimental data. 3. After systemic administration, DL76 was rapidly distributed into all organs studied (liver, kidney, brain, and lung). The highest AUC of DL76 was observed in lungs followed by brain, where the exposure to the investigated compound expressed as AUC was almost 30 times higher than in serum. 4. Bioavailability, calculated based on the area-under-the-concentration–time curve extrapolated to infinity after intravenous and intragastric administration of the dose 3 mg/kg, equalled 60.9%.
Pharmacological Reports | 2006
Ewa Poleszak; Piotr Wlaź; Ewa Kędzierska; Dorota Nieoczym; Elżbieta Wyska; Joanna Szymura-Oleksiak; Sylwia Fidecka; Maria Radziwoń-Zaleska; Gabriel Nowak
Neuropharmacology | 2017
Kinga Sałat; Adrian Podkowa; Natalia Malikowska; Felix T. Kern; Jörg Pabel; Ewelina Wojcieszak; Katarzyna Kulig; Klaus T. Wanner; Beata Strach; Elżbieta Wyska
European Journal of Drug Metabolism and Pharmacokinetics | 2016
Elżbieta Wyska; Artur Świerczek; Krzysztof Pociecha; Katarzyna Przejczowska-Pomierny
European Journal of Medicinal Chemistry | 2018
Grażyna Chłoń-Rzepa; Agnieszka Jankowska; Marietta Ślusarczyk; Artur Świerczek; Krzysztof Pociecha; Elżbieta Wyska; Adam Bucki; Alicja Gawalska; Marcin Kołaczkowski; Maciej Pawłowski
Psychopharmacology | 2018
Aleksandra Szopa; Ewa Poleszak; Urszula Doboszewska; Mariola Herbet; Katarzyna Świąder; Elżbieta Wyska; Anna Serefko; Aleksandra Wlaź; Agnieszka Korga; Marta Ostrowska; Piotr Juś; Szymon Jedynak; Jarosław Dudka; Piotr Wlaź