Zhang Yuqin, Li Huang, Huang Mei, Chu Kedan, Xu Wei, Zhang Shengnan, Que Jinhua, Chen Lidian
College of Pharmacy, Fujian, Fuzhou 350122, PR China; Academy of Integrative Medicine, Fuzhou, Fujian, 350122, PR China.
College of Pharmacy, Fujian, Fuzhou 350122, PR China.
J Ethnopharmacol. 2014 Dec 2;158 Pt A:76-84. doi: 10.1016/j.jep.2014.10.020. Epub 2014 Oct 23.
Gualou Guizhi decoction (GLGZD) prescribed in traditional Chinese medicine has been reported to have protective effects on ischemic stroke. The present study is to investigate the therapeutic effect of GLGZD on ischemic stroke and explore its mode of action.
GLGZD was studied on transient middle cerebral artery occlusion (MCAO) followed by reperfusion in vivo, as well as on hippocampal primary neuron cultures in vitro.
In vivo, it was shown that GLGZD treatment for 7 days could ameliorate transient middle cerebral artery occlusion (MCAO)-induced neurological deficit, histopathology changes and decrease infarct area. Further study demonstrated that GLGZD inhibited over-activation of astrocytes and apoptosis of neurons and GLGZD promoted up-regulation of neuronal specific marker neuron-specific nuclear (NeuN) and microtubule-associated protein 2 (MAP-2) in brain. Moreover, the in vitro study revealed that GLGZD treatment protected against NMDA-induced cell apoptosis and neuronal loss, and promoted up-regulation of neuronal specific marker NeuN.
Taken together, the present study demonstrates that GLGZD produces a protection in the MCAO model rats via inhibiting over-activation of astrocytes, apoptosis of neurons and up-regulation of neuronal specific marker NeuN and MAP-2. Our study reveals that GLGZD might be a potential neuroprotective agent for stroke and can provide basic data for clinical use.
据报道,中医方剂瓜蒌桂枝汤(GLGZD)对缺血性中风具有保护作用。本研究旨在探讨GLGZD对缺血性中风的治疗效果并探索其作用机制。
在体内对GLGZD进行了短暂性大脑中动脉闭塞(MCAO)再灌注研究,以及在体外对海马原代神经元培养物进行了研究。
在体内,结果表明GLGZD连续治疗7天可改善短暂性大脑中动脉闭塞(MCAO)诱导的神经功能缺损、组织病理学变化并减小梗死面积。进一步研究表明,GLGZD抑制星形胶质细胞的过度活化和神经元凋亡,并且GLGZD促进大脑中神经元特异性标志物神经元特异性核蛋白(NeuN)和微管相关蛋白2(MAP-2)的上调。此外,体外研究表明GLGZD处理可防止NMDA诱导的细胞凋亡和神经元丢失,并促进神经元特异性标志物NeuN的上调。
综上所述,本研究表明GLGZD通过抑制星形胶质细胞的过度活化、神经元凋亡以及神经元特异性标志物NeuN和MAP-2的上调,对MCAO模型大鼠产生保护作用。我们的研究表明GLGZD可能是一种潜在的中风神经保护剂,并可为临床应用提供基础数据。