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St. John’s wort (Hypericum perforatum) is one of the popular herbal drugs in Europe and USA. We have recently described benefi cial effects of this herb in the treatment of stress-evoked memory impairments. The aim of the present study was to test a hypothesis that St. John’s wort alleviates stress- and corticosterone-related memory impairments by restoring levels of synaptic plasticity proteins: neuromoduline (GAP-43) and synaptophysin (SYP) in hippocampus and prefrontal cortex. Stressed and corticosterone treated rats presented a signifi cantly delayed acquisition of spatial working memory (P<0.001) in the Barnes maze (BM). Chronic administration of H. perforatum (350 mg kg-1 for 21 days) potently and signifi cantly improved processing of spatial information in the stressed and corticosterone treated rats (P<0.001). Also the herb increased levels of GAP-43 and SYP, in both St. John’s wort treated rat’s hippocampus (P<0.05 and P>0.05, respectively) and prefrontal cortex (P<0.05 and P<0.05) as measured by western immunoblotting. We found that H. perforatum prevented the deleterious effects of both chronic restraint stress and prolonged corticosterone treatment on working memory measured in BM test. These fi ndings indicate that at least part of the benefi cial effect of H. perforatum on memory may be mediated by GAP-43 and SYP proteins.
In this study we advised question whether cerebrospinal fl uid oxidative stress markers are associated with neurotoxicity of chemotherapy of acute lymphoblastic leukaemia (ALL). Examination of 38 ALL patients revealed a statistically signifi cant increase in 8-isoprostane and decrease in total antioxidative capacity during the treatment. Dynamic analysis revealed a statistically signifi cant increase in isoprostane starting on the 59th day of the treatment when the levels were highest and remained raised during all the treatment course. The mean 8-isoprostane level at the diagnosis was 9.05 ± 5.12 pg/ml, and no correlation with initial leukocytosis, organomegaly and lactate dehydrogenase level was noted. Dynamic data analysis revealed a statistically signifi cant increase in 8-isoprostane on the 59th day of the treatment (24.85 ± 26.28) and at four points during consolidation phase (17.28 ± 8.09; 22.72 ± 21.79; 24.92 ± 22.74; 32.32 ± 26.85) as compared to its level at the diagnosis (P<0.01. The mean total antioxidative capacity level at the diagnosis was (203.98 ± 15.11 μmol/l). Dynamic data analysis revealed a statistically signifi cant decrease in total antioxidative capacity on the 59th day of the treatment (189.76 ± 4.64) and at one point during consolidation phase (188.29 ± 8.46) as compared to its level at the diagnosis (P<0.05). The study suggests that standard ALL treatment may cause neurotoxicity by oxidative stress.
In this work we compared in rats the influence of heptapeptide 1-7-angiotensin II, hexapeptide 2-7-angiotensin II, pentapeptide 3-7-angiotensin II and angiotensin II on motility, stereotypy, learning of conditioned avoidance responses and recall of passive avoidance behaviour allowing to avoid aversive stimulation. The 4 peptides administered 15 min before the experiment, tended to increase the number of crossings, rearings and bar approaches in open field, significantly accelerated acquisition of conditioned avoidance responses and improved recall of the passive avoidance. All the peptides applied immediately before the experiment intensified stereotypy evoked by apomorphine in the dose 1 mg/kg and amphetamine in the dose 6.5 mg/kg given intraperitoneally. These results show full psychotropic activity of the examined fragments of angiotensin II, comparable with the activity of the parent octapeptide. Our previous hypothesis that the Val-Tyr-Ile-His-Pro fragment of angiotensin II is responsible for the psychotropic activity evoked by angiotensins in rats is thus confirmed.
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