کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5829968 | 1559012 | 2011 | 7 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Neuropharmacology and AnalgesiaEffects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice Neuropharmacology and AnalgesiaEffects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice](/preview/png/5829968.png)
The present study shows interactive effects of pentoxifylline (PTX) as a phosphodiesterase (PDE) inhibitor, H-89 as a protein kinase A (PKA) inhibitor and bucladesine (db-cAMP) as a cAMP agonist on pentylenetetrazol (PTZ)-induced seizure in mice. Different doses of pentoxifylline (25, 50, 100Â mg/kg), bucladesine (50, 100, 300Â nM/mouse), and H-89 (0.05, 0.1, 0.2Â mg/100Â g) were administered intraperitoneally (i.p.), 30Â min before intravenous (i.v.) infusion of PTZ (0.5% w/v). In combination groups, the first and second components were injected 45 and 30Â min before PTZ infusion. In all groups, the control animals received an appropriate volume of vehicle. Single administration of PTX had no significant effect on both seizure latency and threshold. Bucladesine significantly decreased seizure latency and threshold only at a high concentration (300Â nM/mouse). Intraperitoneal administration of H-89 (0.2Â mg/100Â g) significantly increased seizure latency and threshold in PTZ-treated animals. All applied doses of bucladesine in combination with PTX (50Â mg/kg) caused a significant reduction in seizure latency. Pretreatment of animals with PTX (50 and 100Â mg/kg) attenuated the anticonvulsant effect of H-89 (0.2Â mg/100Â g) in PTZ-exposed animals. H-89 (0.05, 0.2Â mg/100Â g) prevented the epileptogenic activity of bucladesine (300Â nM) with significant increase of seizure latency and seizure threshold. In conclusion, we showed that seizure activities were affected by pentoxifylline, H-89 and bucladesine via interactions with intracellular cAMP and cGMP signaling pathways, cyclic nucleotide-dependent protein kinases, and related neurotransmitters.
Journal: European Journal of Pharmacology - Volume 670, Issues 2â3, 30 November 2011, Pages 464-470