Background Curcumin, an active ingredient of turmeric with antioxidant and anti-inflammatory properties has recently been reported to have anticonvulsant effects in several animal models of epilepsy. This study aimed ...Background Curcumin, an active ingredient of turmeric with antioxidant and anti-inflammatory properties has recently been reported to have anticonvulsant effects in several animal models of epilepsy. This study aimed to investigate the effects of curcumin on the pilocarpine rat model of status epilepticus. Methods The effect of intraperitoneal administration of curcumin （30, 100, and 300 mg/kg） on pilocarpine-induced seizures in rats was tested. The correlation between seizure activity and hippocampal levels of nitric oxide synthase and free radicals was quantified. Whether curcumin treatment modulated these parameters was also investigated. Results Curcumin significantly increased seizure threshold at doses of 100 and 300 mg/kg. Rats with pilocarpine- induced seizures showed significantly elevated levels of malonaldehyde, nitric oxide synthase, and lactate dehydrogenase, but decreased levels of superoxide dismutase and glutathione compared with normal control rats. At doses of 100 and 300 mg/kg, curcumin reversed the effects of pilocarpine-induced seizures on nitric oxide synthase, lactate dehydrogenase, glutathione, and superoxide dismutase. However, curcumin did not restore the elevated malonaldehyde levels. Conclusion Curcumin has anticonvulsant activity in the pilocarpine rat model of seizures, and that modulation of free radicals and nitric oxide synthase may be involved in this effect.展开更多
Determining the minimal duration of status epilepticus （SE） that leads to the development of subsequent spontaneous seizures （i.e., epilepsy） is important, because it provides a critical timewindow for seizure int...Determining the minimal duration of status epilepticus （SE） that leads to the development of subsequent spontaneous seizures （i.e., epilepsy） is important, because it provides a critical timewindow for seizure intervention and epilepsy prevention. In the present study, male ICR （imprinting Control Region） mice were injected with pilocarpine to induce acute sei zures. SE was terminated by diazepam at 10 min, 30 min, 1 h, 2 h and 4 h after seizure onset. Spon taneous seizures occurred in the 1, 2 and 4 h SE groups, and the seizure frequency increased with the prolongation of SE. Similarly, the Morris water maze revealed that the escape latency was significantly increased and the number of target quadrant cross ings was markedly decreased in the 1, 2 and 4 h SE groups. Robust mossy fiber sprouting was observed in these groups, but not in the 10 or 30 min group. In contrast, FluoroJade B staining revealed significant cell death only in the 4 h SE group. The incidence and frequency of spontaneous seizures were corre lated with Timm score （P = 0.004） and escape latency （P = 0.004）. These data suggest that SE longer than one hour results in spontaneous motor seizures and memory deficits, and spontaneous seizures are likely associated with robust mossy fiber sprouting but not neuronal death.展开更多
文摘Background Curcumin, an active ingredient of turmeric with antioxidant and anti-inflammatory properties has recently been reported to have anticonvulsant effects in several animal models of epilepsy. This study aimed to investigate the effects of curcumin on the pilocarpine rat model of status epilepticus. Methods The effect of intraperitoneal administration of curcumin （30, 100, and 300 mg/kg） on pilocarpine-induced seizures in rats was tested. The correlation between seizure activity and hippocampal levels of nitric oxide synthase and free radicals was quantified. Whether curcumin treatment modulated these parameters was also investigated. Results Curcumin significantly increased seizure threshold at doses of 100 and 300 mg/kg. Rats with pilocarpine- induced seizures showed significantly elevated levels of malonaldehyde, nitric oxide synthase, and lactate dehydrogenase, but decreased levels of superoxide dismutase and glutathione compared with normal control rats. At doses of 100 and 300 mg/kg, curcumin reversed the effects of pilocarpine-induced seizures on nitric oxide synthase, lactate dehydrogenase, glutathione, and superoxide dismutase. However, curcumin did not restore the elevated malonaldehyde levels. Conclusion Curcumin has anticonvulsant activity in the pilocarpine rat model of seizures, and that modulation of free radicals and nitric oxide synthase may be involved in this effect.
基金supported by grants from the National Nature Science Foundation of China (8107262)the Zhejiang Provincial Natural Science Foundation of China (Y2100417)+1 种基金the Foundation of Qianjiang Talents (QJD1002012)the Foundation of Health Department of Zhejiang Province for Outstanding Youths (2010)
文摘Determining the minimal duration of status epilepticus （SE） that leads to the development of subsequent spontaneous seizures （i.e., epilepsy） is important, because it provides a critical timewindow for seizure intervention and epilepsy prevention. In the present study, male ICR （imprinting Control Region） mice were injected with pilocarpine to induce acute sei zures. SE was terminated by diazepam at 10 min, 30 min, 1 h, 2 h and 4 h after seizure onset. Spon taneous seizures occurred in the 1, 2 and 4 h SE groups, and the seizure frequency increased with the prolongation of SE. Similarly, the Morris water maze revealed that the escape latency was significantly increased and the number of target quadrant cross ings was markedly decreased in the 1, 2 and 4 h SE groups. Robust mossy fiber sprouting was observed in these groups, but not in the 10 or 30 min group. In contrast, FluoroJade B staining revealed significant cell death only in the 4 h SE group. The incidence and frequency of spontaneous seizures were corre lated with Timm score （P = 0.004） and escape latency （P = 0.004）. These data suggest that SE longer than one hour results in spontaneous motor seizures and memory deficits, and spontaneous seizures are likely associated with robust mossy fiber sprouting but not neuronal death.
