Nimodipine attenuates the convulsion of pentylenetetrazoloe-induced status epilepsy with increasing expression of phosphated-ERK in the hippocampus of rats
Lijing Jia, Shiping Li, Tao Xie, Junli Zhen, Zhou-ping Li
Abstract
Lijing Jia, Shiping Li, Tao Xie, Junli Zhen, Zhou-ping Li
Abstract
Objective To detect the expression of extracellular-regulated kinase (ERK)and phosphated-extracellular-regulated kinase(P-ERK) in the hippocampus after pentylenetetrazoloe-induced status epilepsy and the effects of nimodipine on it. Methods Male Sprague-Dawley adult rats (200-250 g) were randomly divided into normal control group(NC, n=35), status epilepsy group (SE, n=40), nimodipine group (NIM, n=40). The rats were injected first with 40 mg/kg pentylenetetrazoloe(PTZ), followed 10 minutes later by 20 mg/kg PTZ, and subsequently, 10 mg/kg PTZ ip every 10 minutes until SE occurred, apoint charactered by a loss of postural control and tonic-clonic seizures.Rats in control group received the same number of saline injections.Rats in NIM group were injected NIM(2.5 mg/kg) intraperitoneally 15 min before the injection of PTZ.Rats in every group were killed at 30 minutes, 1 hour, 3 hours , 12 hours, 24 horus, 72 hours and 7 days after status epilepsy respectively and the hippocampus were dissected.The expression of ERK and P-ERK in the hippocampus were detected by Western blot. Results Nimodipine attenuated the convulsion of PTZ-induced status epilepsy.There was dynamic expression of P-ERK in SE group.In NIM group, the expression of P-ERK was markedly increased than that of SE group at 30 min, 1h, 3h, 12h, 24h, 72h, and 7d (3.26±0.95 vs 2.56±0.82 at 30 min, P<0.05). Conclusion Nimodipine attenuates the convulsion of PTZ-induced status epilepsy with increased expression of phosphated-ERK in the hippocampus of rats. Key words: Epilepsy; Pentylenetetrazol; Nimodipine; Mitogen-activated protein kinase/ extracellular- regulated kinase
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Objective To detect the expression of extracellular-regulated kinase (ERK)and phosphated-extracellular-regulated kinase(P-ERK) in the hippocampus after pentylenetetrazoloe-induced status epilepsy and the effects of nimodipine on it. Methods Male Sprague-Dawley adult rats (200-250 g) were randomly divided into normal control group(NC, n=35), status epilepsy group (SE, n=40), nimodipine group (NIM, n=40). The rats were injected first with 40 mg/kg pentylenetetrazoloe(PTZ), followed 10 minutes later by 20 mg/kg PTZ, and subsequently, 10 mg/kg PTZ ip every 10 minutes until SE occurred, apoint charactered by a loss of postural control and tonic-clonic seizures.Rats in control group received the same number of saline injections.Rats in NIM group were injected NIM(2.5 mg/kg) intraperitoneally 15 min before the injection of PTZ.Rats in every group were killed at 30 minutes, 1 hour, 3 hours , 12 hours, 24 horus, 72 hours and 7 days after status epilepsy respectively and the hippocampus were dissected.The expression of ERK and P-ERK in the hippocampus were detected by Western blot. Results Nimodipine attenuated the convulsion of PTZ-induced status epilepsy.There was dynamic expression of P-ERK in SE group.In NIM group, the expression of P-ERK was markedly increased than that of SE group at 30 min, 1h, 3h, 12h, 24h, 72h, and 7d (3.26±0.95 vs 2.56±0.82 at 30 min, P<0.05). Conclusion Nimodipine attenuates the convulsion of PTZ-induced status epilepsy with increased expression of phosphated-ERK in the hippocampus of rats. Key words: Epilepsy; Pentylenetetrazol; Nimodipine; Mitogen-activated protein kinase/ extracellular- regulated kinase
Key concepts: Nimodipine, Epilepsy, Convulsion, Hippocampus, Medicine, Saline, MAPK/ERK pathway, Anesthesia