Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Añadir filtros








Intervalo de año
1.
Journal of Sabzevar University of Medical Sciences. 2011; 18 (4): 235-242
en Persa | IMEMR | ID: emr-180022

RESUMEN

Background and Purpose: Ethanol is known as anticonvulsant and proconvulsant but sometimes has no effect on seizure. There is no report about the role of ethanol on the anticonvulsant effect of Valproic acid [VPA]. In this study, we explore the effect of ethanol on the anticonvulsant effect of VPA


Methods and Materials: In this experimental study, eight groups of mice [25-30 gr] were injected pentylenetetrazol [PTZ] [37mg/kg; ip] every other day [3 times a week]. Groups receiving ethanol [0.5 and 1 g/kg; 7 and 21 continuous days; everyday; ip], PTZ was injected 30 minutes after ethanol. In Valproic acid+ethanol, Valproic acid [100 mg/kg] was injected 5 minutes before ethanol [1 g/kg]. Immediately after PTZ injection, seizure stages were recorded for 20 min. Seizure stage-4 duration [S4D], seizure stage-4 latency [S4L] and seizure stage 1 latency [S1L] were recorded from each mouse after PTZ injection, and data were compared with control groups. The basis of all decisions was a significant level of P<0.05. Data analysis was done in Statistica 5.5


Results: Pretreatment of animals with ethanol [1 g/kg for 7 days] decreased cumulative [c] S4D [%31.8 PTZ+Saline]; and with ethanol [1 g/kg for 21 days] decreased cS4D [%48.3 PTZ+Saline] [P<0.001], but increased cS4L [%112.6 PTZ+Saline] and cSL [%116.8 PTZ+Saline] significantly [P<0.001]. Pretreatment of animals with VPA [100 mg/kg] significantly decreased cumulative [c] S4D [%39 PTZ+Saline] [P<0.001], and significantly increased cS4L [%216.8 PTZ+Saline] and cS1L [%149 PTZ+Saline] [P<0.001]. Intraperitoneal injection of VPA+ethanol significantly decreased cS4D [%56.1 relative to PTZ+VPA and %46.1 relative to PTZ+Eth 1 [7]] [P<0.001]; it also increased cS4L [%233.9 relative to PTZ+VPA and %450 relative to PTZ+Eth1 [7]] [P<0.001], but had no effect on cS1L as compared to VPA and ethanol [1 g/kg; 7 days]


Conclusion: The results indicated that ethanol [1 g/kg] functions not only as an anticonvulsant but its simultaneous injection [7 continuous days] also enhances the anticonvulsant effects of valproic acid

2.
Journal of Sabzevar University of Medical Sciences. 2009; 16 (2): 62-71
en Persa | IMEMR | ID: emr-179977

RESUMEN

Background and purpose: Antioxidants and vitamin D3 are currently used for the treatment of neurodegenerative diseases although their mechanism of action is not well understood. The present study was conducted to investigate the effect of combined administration of vitamins D3 and E on demyelination, cell death and remyelination of rat hippocampus following the local ethidium bromide [EB] injection


Methods and Materials: This experimental study was conducted on 32 Spague rats. After EB-induced demyelination, animals received intraperitoneal vitamin E [100 mg/kg] and D3 [5microg/kg] together for 7 days. The extent and intensity of demyelination were studied by luxol fats blue staining, the activated caspase-3 genes and MBP. The study data were analyzed in SPSS using one-way ANOVA and Tukey post test


Results: The findings revealed that the combined administration of vitamins E and D3 for 7 days caused a significant reduction in the expression of activated caspase-3 [10 +/- 0] [p<0.001], as well as a significant increase in MBP expression [236 +/- 30] [p<0.001]. EB injection alone significantly increased demylination [p<0.05]. Combined administration of the two vitamins significantly reduced the extent of demyelination [0.1 +/- 0.03] [p<0.05], and increased remyelination intensity [0.6 +/- 0.06] [p<0.05]


Conclusion: The results of the present study indicated that the combined administration of vitamins E and D3 reduced EB induced demyelination and apopthosis, and improved remyelination

3.
Journal of Sabzevar University of Medical Sciences. 2008; 15 (3): 129-137
en Persa | IMEMR | ID: emr-179961

RESUMEN

Background and Purpose: Previous studies have not properly clarified the role of A2A adenosine receptors in convulsions induced by kindling. In the present study, the role of these receptors in convulsions induced perforant path kindling has been investigated by blocking these receptors [with specific antagonists]


Methods and Materials: This experimental study was conducted on 24 rats which were randomly divided into four groups of six. They were kindled by electric stimulation of the perforant path. In two groups, before each kindling stimulation, antagonists of A2A adenosine receptors [ZM 241385] [500 and 200 =M] was injected to the lateral ventricle of the rats. Control animals were given only the electric stimulations. In the fourth group [sham], the solvent of the abovementioned drug was injected to the lateral ventricle before kindling stimulations. The obtained data were analyzed using two-way ANOVA and Tukey tests


Results: Injecting the antagonists of A2A adenosine receptors [ZM 241385] [500 =M] to the lateral ventricle of the rats postponed the process of kindling. Two-way ANOVA indicated that number of stimulations required to reach the convulsive stages were significantly increased [P<0.001, F[4, 40] = 47]. Also, compared with the sham group which received the solvent of the drug, a significant reduction was observed in the duration of depletion waves following accumulation [P<0.05, F[6, 60] = 2.5] in this group


Conclusion: According to the findings, injecting the antagonists of A2A adenosine receptors produces a significant anticonvulsant effect on the convulsions induced by perforant path kindling, and that this effect functions through controlling the effect of endogenic adenosine on A2A adenosine receptors

SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA