Honokiol, a neuroprotectant against mouse cerebral ischaemia, mediated by preserving Na+, K+-ATPase activity and mitochondrial functions
Honokiol, a neuroprotectant against mouse cerebral ischaemia, mediated by preserving Na+, K+-ATPase activity and mitochondrial functions
复制标题
DOI：
10.1111/j.1742-7843.2007.00082.x
复制
发表时间：
2007-08-01
影响因子：
3.1
通讯作者：
Lin-Shiau, Shoei-Yn
中科院分区：
文献类型：
--
作者：
Chen, Chang-Mu;Liu, Shing-Hwa;Lin-Shiau, Shoei-Yn
厚朴酚是草本植物厚朴的一种成分，具有抗氧化、抗炎和抗焦虑的特性，能提高癫痫发作阈值，促进神经突起生长。由于中风已成为工业化国家的第二大死亡原因，因此迫切需要一种有效的神经保护剂。在本研究中，我们试图在小鼠脑缺血模型中阐明本木酚是否可能是一种神经保护剂。将成年雄性癌症研究所（ICR）小鼠置于大脑中动脉闭塞45分钟。在缺血诱导前15分钟和缺血诱导后60分钟，分别腹腔注射厚木酚（10 μ g/kg， 0.2 ml生理盐水中）或对照组2次。该方法诱导的脑缺血与突触体活性氧产生的增加、突触体线粒体膜电位（δ Psi m）和突触体线粒体代谢功能的降低以及从选定脑区分离的组织中Na+、K+- atp酶活性的降低有关。给予厚朴酚可显著减少脑梗死体积和突触体活性氧的产生。在缺血脑组织中观察到的突触体线粒体膜电位、突触体线粒体代谢功能和组织Na+、K+- atp酶活性的下降也被厚木酚所减弱。由此可见，厚朴酚具有保护脑缺血再灌注损伤和线粒体氧化应激功能的作用。关于治疗应用，需要进一步的研究来评估其在临床中的有效性和安全性。
Honokiol, a component of the herb Magnolia offzcinalis, exhibits antioxidant, anti-inflammatory and anxiolytic properties, increases seizure threshold, and promotes neurite outgrowth. Because stroke has become the second leading cause of death in industrialized countries, an effective neuroprotectant is urgently required. In this study, we attempted to elucidate in a mouse cerebral ischaemia model whether honokiol could be a neuroprotectant. Adult male Institute of Cancer Research (ICR) mice were subjected to middle cerebral artery occlusion for 45 min. Honokiol (10 mu g/kg in 0.2 ml of saline) or control vehicle was intraperitoneally administered twice, 15 min. before and 60 min. after the induction of ischaemia. Cerebral ischaemia induced by this method was associated with an increase in synaptosomal production of reactive oxygen species, with decreases in synaptosomal mitochondrial membrane potential (Delta Psi m) and synaptosomal mitochondrial metabolic function, and with reductions in Na+, K+-ATPase activities of tissues isolated from selected brain regions. Administration of honokiol resulted in significant reductions in brain infarct volume and in synaptosomal production of reactive oxygen species. The decreases in synaptosomal mitochondrial membrane potential, synaptosomal mitochondrial metabolic function and tissue Na+, K+-ATPase activities observed in the ischaemic brains were also attenuated by honokiol treatments. It is concluded that honokiol can protect brain against ischaemic reperfusion injury and preserve mitochondrial function from oxidative stress. Regarding therapeutic application, further studies are needed to assess the efficacy and safety of honokiol in clinical situations.