Polish journal of pharmacology最新文献

{"title":"Influence of Casearia esculenta root extract on protein metabolism and marker enzymes in streptozotocin-induced diabetic rats.","authors":"A Prakasam,&nbsp;S Sethupathy,&nbsp;K V Pugalendi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The present study investigated the possible protective effects of Casearia esculenta root extract on certain biochemical markers in streptozotocin (STZ)-induced diabetes in rats. STZ treatment (50 mg/kg, ip) caused a hyperglycemic state, that led to various physiological and biochemical alterations. Blood levels of glucose, urea, uric acid and creatinine, plasma levels of albumin and albumin/globulin ratio and the activities of diagnostic marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (gamma-GT) in plasma, liver and kidney were markedly altered in STZ diabetic rats. Oral administration of C. esculenta (200 and 300 mg/kg) for 45 days restored all these biochemical parameters to near normal levels. Thus, the present results have shown that C. esculenta root extract has the antihyperglycemic effect and consequently may alleviate liver and renal damage associated with STZ-induced diabetes in rats.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"587-93"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of nonselective and selective opioid receptors antagonists on antinociceptive action of acetaminophen [part III].","authors":"M Bujalska","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The influence of naloxone (NAL), a competitive antagonist of mu, kappa, delta and sigma receptors; D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH(2) (CTOP), selective antagonist of mu-opioid receptors; nor-binaltorphimine (NOR-BNI), a potent and higly selective kappa opioid receptor antagonist; naltrindole (NTI), a delta-opioid receptor antagonist and naltriben (NTB), a highly selective delta(2)-opioid receptor antagonist on antinociceptive action of acetaminophen (ACETA) was studied in rats. NAL administered intraperitoneally (ip) or intracerebroventricularly (icv), and CTOP and NOR-BNI administered icv, markedly decreased the antinociceptive activity of the high dose of ACETA (400 mg/kg). Pretreatment with NTI (sc), as well as with naloxone (it), and NTB (it) slightly but significantly attenuated the ACETA antinociception. The possible involvement of the opioidergic systems in antinociceptive activity of ACETA is discussed.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"539-45"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell cycle arrest induced in human breast cancer cells by cyclin-dependent kinase inhibitors: a comparison of the effects exerted by roscovitine and olomoucine.","authors":"J Wesierska-Gadek,&nbsp;M Gueorguieva,&nbsp;J Wojciechowski,&nbsp;M Horky","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cyclin-dependent kinases (CDKs) are serine/threonine kinases that play a key role in the regulation of the cell cycle progression. In proliferating cells, distinct CDKs activated upon complexing with specific cyclins and upon site-specific phosphorylation coordinate in an orchestrated way the appropriate transition between consecutive phases of the cell cycle. Aberrant expression or altered activity of distinct CDK complexes results in escape of cells from the cell cycle control and leads to malignant transformation. Therefore, the inhibition of CDKs in malignant cells provides a new strategy in the fight against cancer. Recently, selective CDK inhibitors targeting distinct CDKs were developed. They represent promising anti-cancer drugs due to their strong anti-proliferative efficacy combined with a relative low direct cytotoxicity. The aim of this study was to compare the effect of two related CDK inhibitors: roscovitine (ROSC) and olomoucine (OLO) on the cell cycle progression in human breast cancer MCF-7 cells. Both examined CDK inhibitors differentially affected the cell cycle progression in MCF-7 cels. Whereas ROSC arrested cells in G(2)/M, OLO inhibited cells at S to G(2) transition and increased the number of cells residing in the S-phase. Moreover, both CDK inhibitors modulated the cell cycle progression with distinct kinetics. Accumulation of G(2)/M-arrested cells beginning 6 h after exposure of cells to ROSC coincided with a strong up-regulation of the p53. Interestingly, ROSC triggered apoptosis in MCF-7 cells by activation of mitochondrial pathway. Loss of the integrity of mitochondrial membrane observed after exposure of cells to ROSC for 6 h led to release of distinct mitochondrial proteins, e.g. apoptosis inducing factor (AIF). In contrast to ROSC, OLO-induced cell cycle changes could be detected after 12 h of the treatment. OLO did not up-regulate p53 protein. It indicates that both examined CDK inhibitors are selective and block the cell cycle progression of human breast carcinoma cells at different phases.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"635-41"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of the nitric oxide donor and the nitric oxide synthase inhibitor on the liver of rats with chronic hepatitis induced by dimethylnitrosamine.","authors":"O Lukivskaya,&nbsp;R Lis,&nbsp;K Zwierz,&nbsp;V Buko","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The present study was designed to examine the effects of the donor of nitric oxide (NO), NaNO(2) and the inhibitor of NO synthase, N(omega)-nitro-L-arginine (L-NNA), on the development of dimethylnitrosamine (DMNA)-induced chronic hepatitis in rats. L-NNA decreased rat survival and enhanced the severity of hepatic encephalopathy in the DMNA-treated animals. The aggravation of the morphological signs of hepatitis, the activation of serum alanine aminotransferase and cytosolic superoxide dismutase activities and the increase in the liver malondialdehyde content were observed in this group. The treatment with NaNO(2) improved liver morphology, decreased serum marker enzyme activities, lowered the activities of alpha-D-mannosidase and N-acetyl-beta-D-glucosaminidase compared to the DMNA-treated group. The results of the morphological and biochemical studies suggest that L-NNA increased DMNA-induced liver damage, whereas NaNO(2) partially prevented the development of chronic hepatitis. It is proposed that the opposite effects of L-NNA and NaNO(2) are partially explained by a modulation of the free radical-dependent processes in the liver.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"599-604"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of MPEP, a selective mGluR5 antagonist, on the antielectroshock activity of conventional antiepileptic drugs.","authors":"M Zadrozniak,&nbsp;A Sekowski,&nbsp;S J Czuczwar,&nbsp;K K Borowicz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>MPEP, a selective non-competitive antagonist of group I metabotropic glutamate receptor subtype 5 (mGluR5), administered at doses ranging from 0.75 to 1 mg/kg, failed to influence the electroconvulsive threshold in mice. However, when administered at higher doses (1.25 and 1.5 mg/kg), it significantly increased the threshold. Moreover, MPEP (applied at its highest subprotective dose of 1 mg/kg) did not affect the protective action of valproate, carbamazepine, diphenylhydantoin and phenobarbital against maximal electroshock-induced seizures in mice. The presented results indicate that mGluR5 antagonists should not be considered as good candidates for add-on therapy of generalized seizures.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"595-8"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flupentixol and trifluperidol reduce interleukin-1 beta and interleukin-2 release by rat mixed glial and microglial cell cultures.","authors":"J Kowalski,&nbsp;K Labuzek,&nbsp;Z S Herman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neuroleptics penetrate into the brain, where they act not only on neurons but probably also on glial cells. In the available literature, there are no reports on the effect of neuroleptics on cytokine release in glia cultures. The aim of this study was to evaluate the effect of neuroleptics on the release of proinflammatory cytokines (IL-1beta and IL-2) by mixed glial and microglial cell cultures. Trifluperidol at 20 and 2 muM reduced IL-beta secretion by mixed glial cultures after 3 days of exposure. Trifluperidol at 20, 2 and 0.2 muM diminished IL-beta secretion after 1 day of incubation. Trifluperidol at 20 and 2 muM reduced IL-2 release after 1 and 3 days of exposure. Flupentixol at 20 and 2 muM reduced IL-1beta by mixed glial cell cultures after 3 days of exposure. Flupentixol at 20, 2 and 0.2 muM caused diminution of IL-1beta release after 1 day of exposure. Flupentixol at 20 and 2 muM reduced IL-2 release after 1 day of incubation. Flupentixol at 20, 2 and 0.2 muM diminished IL-2 release after 3 days of exposure. Flupentixol at 20, 10, 2 and 0.2 muM reduced IL-1beta release by microgial cell cultures. Flupentixol at 20, 10 and 2 muM reduced release of IL-2 by microglial cells after 1 day of exposure. The results of the present study suggest that neuroleptics have an inhibiting effect on the release of glial cytokines, but clinical significance this results remains to be elucidated.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"563-70"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of nitric oxide synthase prevents energy failure and oxidative damage evoked in the brain by lipopolysaccharide.","authors":"G A Czapski,&nbsp;M Cakała,&nbsp;D Kopczuk,&nbsp;M Kamińska,&nbsp;J B Strosznajder","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The inducible nitric oxide synthase (iNOS) plays an important role in endotoxic shock. However,little is known about the involvment of constitutive isoform(s) of NOS (cNOS). The aim of this study was to determine the role of cNOS in the mouse brain after lipopolysaccharide (LPS) injection. Concentrations of nicotinamide adenine dinucleotide (NAD(+)), carbonyl group and thiobarbituric acid reactive substances were determined spectrophotometrically, cNOS mRNA was evaluated by RT-PCR. Our data showed that LPS significantly decreased NAD(+) level, and enhanced protein and lipid oxidation, but had no effect on cNOS mRNA expression. Inhibitors of cNOS protected the cells against alterations evoked by LPS, suggesting involvement of cNOS isoforms in pathology.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"643-6"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective role of testosterone in the nervous system.","authors":"M Białek,&nbsp;P Zaremba,&nbsp;K K Borowicz,&nbsp;S J Czuczwar","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Testosterone -- the gonadal sex steroid hormone plays an important role in the central nervous system (CNS) development. One of the less known testosterone actions is neuroprotection. There are some evidences supporting the hypothesis that testosterone may act protectively in neurodegenerative disorders, e.g. Alzheimer's disease (AD), mild cognitive impairment (MCI) or depression. Androgens alter also the morphology, survival and axonal regeneration of motor neurons. These hormones accelerate the regeneration of hamster facial nerve and anterior tibialis sciatic nerve in rabbits following crush axotomy. Androgens exert trophic action in laryngeal motor nucleus of Xenopus laevis. Testosterone is linked to an increase in neuron somal size, neuritic growth, plasticity and synaptogenesis in both motoneurons of the spinal nucleus of the bulbocavernosus and several populations of pelvic autonomic neurons. The hormone reduced the extent of spinal cord damage in vitro. There are also evidences against the neuroprotective action of testosterone. Testosterone does not protect against methamphetamine-induced neurotoxicity of the dopaminergic system in mice and does not provide significant neuroprotection against glutamate-induced neurotoxicity. Androgens do not prevent striatal dopamine depletion induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice. Although the role of testosterone in the CNS is still poorly understood, accumulating evidence suggests that testosterone may create a future treatment for MCI and related cognitive diseases, including dementia and may influence motor neuron regeneration in adulthood. Androgen replacement therapy in selected male populations may hold therapeutic promise for the prevention and/or treatment of age-related disorders associated with neuronal injury.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"509-18"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of topiramate on the kainate-induced status epilepticus, lipid peroxidation and immunoreactivity of rats.","authors":"M Kubera,&nbsp;B Budziszewska,&nbsp;L Jaworska-Feil,&nbsp;A Basta-Kaim,&nbsp;M Leśkiewicz,&nbsp;M Tetich,&nbsp;M Maes,&nbsp;G Kenis,&nbsp;A Marciniak,&nbsp;S J Czuczwar,&nbsp;G Jagła,&nbsp;W Nowak,&nbsp;W Lasoń","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Topiramate, a new anticonvulsant, has been reported to possess neuroprotective effects in both in vivo and in vitro experiments. In the present study, the effect of topiramate (40 and 80 mg/kg ip) on the fully developed kainate-induced status epilepticus was evaluated in the rat. Injection of kainate (15 mg/kg ip) evoked recurrent limbic seizures which lasted several hours. Topiramate injected 1.5 h after kainate administration had no effect on the seizures and mortality of the animals. Biochemical study revealed that at 80 mg/kg ip, topiramate significantly attenuated the kainate-induced lipid peroxidation in the piriform cortex and showed similar tendency in the frontal cortex. Besides the central nervous system, the kainate-induced seizures evoked significant changes in immunoreactivity, such as reduction in thymus weight and the proliferative activity of splenocytes, and the splenocyte-increased production of interleukin-10, but not interferon-gamma. Topiramate did not affect the kainate-induced reduction in thymus weight, but attenuated changes in the proliferative activity of splenocytes. It is concluded that topiramate, when given during the fully developed kainate-induced status epilepticus in rats, has no effect on seizures, but attenuates lipid peroxidation in piriform cortex and prevents certain changes in immunoactivity.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"553-61"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anxiolytic- and antidepressant-like effects of 7-OH-DPAT, preferential dopamine D3 receptor agonist, in rats.","authors":"Z Rogóz,&nbsp;G Skuza,&nbsp;A Kłlodzińska","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aim of the present study was to examine a potential anxiolytic- and antidepressant-like action of (+)-7-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (7-OH-DPAT), a preferential dopamine D(3) receptor agonist, and N-{4-[4-(2-methoxyphenyl)-1-piperazinyl]butyl}-2-naphthylcarboxamide (BP 897), a partial dopamine D(3) receptor agonist, in male Wistar rats. Diazepam or imipramine were used as reference compounds. The anxiolytic-like effect of those drugs was tested in the elevated plus-maze test. The antidepressant-like effect was estimated using the forced swimming test. The obtained results showed that 7-OH-DPAT at low doses and BP 897 (like diazepam) induced anxiolytic-like effects in the elevated plus-maze test. 7-OH-DPAT, BP 897 and diazepam, tested at the doses effective in the model of anxiolytic-like actions, did not affect motor coordination. Moreover, 7-OH-DPAT at higher doses, like imipramine, showed antidepressant-like effect, significantly reducing immobility time in the forced swimming test. Combined treatment with 7-OH-DPAT and imipramine induced a stronger effect in Porsolt's test than administration of either drug alone, but did not increase the locomotor activity. In contrast, BP 897 was inactive in the forced swimming test when given alone but it potentiated the antidepressant-like effect of imipramine. These data suggest that preferential D(3) receptor agonists may play a role in the therapy of anxiety and/or depression, however, further studies are necessary to elucidate the mechanism of these actions.</p>","PeriodicalId":20292,"journal":{"name":"Polish journal of pharmacology","volume":"56 5","pages":"519-26"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24855459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}