Zhang Yuqin, Li Huang, Huang Mingqing, Huang Mei, Chu Kedan, Xu Wei, Zhang Shengnan, Que Jinhua, Chen Lidian
College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P. R. China.
Am J Chin Med. 2015;43(3):543-57. doi: 10.1142/S0192415X15500342.
Paeoniflorin (PF) is a principal bioactive component, which exhibits many pharmacological effects, including protection against ischemic injury. This paper aimed to investigate the protective effect of PF both in vivo and in vitro. Middle cerebral artery occlusion (MCAO) was performed on male Sprague-Dawley (SD) rat for 2 h, and different doses of PF or vehicle were administered 2 h after reperfusion. Rats were sacrificed after 7 days treatment of PF/vehicle. PF treatment for 7 days ameliorated MCAO-induced neurological deficit and decreased the infarct area. Further study demonstrated that PF inhibited the over-activation of astrocytes and apoptosis of neurons, and PF promoted up-regulation of neuronal specific marker neuron-specific nuclear (NeuN) and microtubule-associated protein 2 (MAP-2) in brain. Moreover, NMDA-induced neuron apoptosis was employed. The in vitro study revealed that PF treatment protected against NMDA-induced cell apoptosis and neuronal loss via up-regulation of neuronal specific marker NeuN, MAP-2 and Bcl-2 and the down-regulation Bax. Taken together, the present study demonstrates that PF produces its protective effect by inhibiting the over-activation of astrocytes, apoptosis of neurons and up-regulation of neuronal specific marker NeuN, MAP-2, and B-cell lymphoma-2 (Bcl-2), and down-regulation Bax. Our study reveals that PF may be a potential neuroprotective agent for stroke and can provide basic data for clinical use.
芍药苷(PF)是一种主要的生物活性成分,具有多种药理作用,包括对缺血性损伤的保护作用。本文旨在研究PF在体内和体外的保护作用。对雄性Sprague-Dawley(SD)大鼠进行大脑中动脉闭塞(MCAO)2小时,再灌注2小时后给予不同剂量的PF或溶剂。给予PF/溶剂处理7天后处死大鼠。PF处理7天可改善MCAO诱导的神经功能缺损并减小梗死面积。进一步研究表明,PF可抑制星形胶质细胞的过度活化和神经元凋亡,并且PF可促进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,采用N-甲基-D-天冬氨酸(NMDA)诱导的神经元凋亡。体外研究表明,PF处理可通过上调神经元特异性标志物NeuN、MAP-2和B细胞淋巴瘤-2(Bcl-2)以及下调Bax来保护细胞免受NMDA诱导的凋亡和神经元丢失。综上所述,本研究表明PF通过抑制星形胶质细胞的过度活化、神经元凋亡以及上调神经元特异性标志物NeuN、MAP-2和B细胞淋巴瘤-2(Bcl-2)并下调Bax发挥其保护作用。我们的研究表明PF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。