Wang Sheng-jun, Wang Shu-hua, Song Zhao-feng, Liu Xue-wu, Wang Rong, Chi Zhao-fu
Department of Neurology, Qilu Hospital of Shandong University, China.
Neuroreport. 2007 Aug 6;18(12):1285-9. doi: 10.1097/WNR.0b013e32826fb3a5.
3-Aminobenzamide (3-AB), an inhibitor of poly(ADP-ribose) polymerase (PARP), has been proved to have neuroprotective properties. In this study, we examined the role of 3-AB in rat hippocampal neuron death induced by seizures. Our data showed that the seizures resulted in PARP activation and translocation of the apoptosis-inducing factor from the mitochondria to the nucleus, leading to neuron death. These effects could, however, all be abolished by 3-AB. Moreover, we showed that 3-AB facilitated Akt activation and decreased the activity of its downstream target, glycogen synthase kinase-3beta. Altogether, our data suggested that 3-AB might have a therapeutic value in seizure-induced hippocampal neuron damage, probably due to the inhibition of apoptosis and activation of Akt cell survival signaling.
3-氨基苯甲酰胺(3-AB)是聚(ADP-核糖)聚合酶(PARP)的抑制剂,已被证明具有神经保护特性。在本研究中,我们检测了3-AB在癫痫诱导的大鼠海马神经元死亡中的作用。我们的数据显示,癫痫发作导致PARP激活以及凋亡诱导因子从线粒体转位至细胞核,从而导致神经元死亡。然而,这些效应均可被3-AB消除。此外,我们发现3-AB促进了Akt激活并降低了其下游靶点糖原合酶激酶-3β的活性。总之,我们的数据表明,3-AB可能对癫痫诱导的海马神经元损伤具有治疗价值,这可能是由于其抑制了细胞凋亡并激活了Akt细胞存活信号通路。