【摘 要】
：
The pathophysiologic mechanisms of epileptogenesis are still poorly understood and there was still no effective therapy available to suppress epileptogenesis.Significant β-nicotinamide adenine dinucle
【机 构】
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Bio-x Institute,School of Life Sciences and Biotechnology,Shanghai Jiao Tong University,Shanghai,200
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
The pathophysiologic mechanisms of epileptogenesis are still poorly understood and there was still no effective therapy available to suppress epileptogenesis.Significant β-nicotinamide adenine dinucleotide(NAD+)depletion,inactivation of sirt1,augment of Acp53/p53,neuronal apoptosis of hippocampus were detected in PILO-induced SE mice in early-stage epileptogenesis.Here,NAD+was used to treat Pilocarpine(PILO)-induced status epilepticus(SE)mice within 24 h after SE.NAD+treatment significantly decreased the incidence of spontaneous recurrent seizures(SRS),abnormal EEG activity,and impaired contextual fear memory formation.NAD+supply distinctly reversed the depletion of endogenous NAD+,inactivation of sirt1,and augment of Acp53/p53.Moreover,neuronal apoptosis was suppressed.The results suggested that early-stage NAD+supplement inhibited epileptogenesis by suppressing neuronal apoptosis through sirt1-Ap53/p53 pathway.
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