Department of Neurobiology, Southern Medical University, 1023S Shatai Road, Guangzhou 510515, China.
J Ethnopharmacol. 2010 Jan 8;127(1):38-46. doi: 10.1016/j.jep.2009.09.054. Epub 2009 Oct 2.
Xiao-Xu-Ming decoction (XXMD) has long been employed clinically to treat stroke in traditional Chinese Medicine.
To investigate the neuroprotective effects of XXMD in vivo and in vitro stroke models and determine involved mechanisms.
Two models (four-vessel occlusion in adult Wistar rats and oxygen-glucose deprivation primary cultured neurons) were employed to mimic ischemia-reperfusion damage, in vivo and in vitro, respectively. The effects of XXMD were investigated with respect to neuronal damage, activity of caspase-3 and expression of Bcl-2 in CA1 region of hippocampus after ischemia. The cognitive ability was measured 7 days after ischemia/reperfusion by using Morris water maze.
Oral administration of XXMD significantly increased the density of neurons that survived in the CA1 region of hippocampus on the 3rd and 7th day after transient global ischemia was induced in a dose-dependent manner. XXMD ameliorated severe deficiencies in spatial cognitive performance induced by transient global ischemia. Inhibition of caspase-3 activity and up-regulation of Bcl-2 expression were induced in the high dose of XXMD-treated rats after ischemia. In oxygen-glucose deprivation model, both XXMD extract and drug-containing serum prepared from blood of high dose of XXMD-treated rats inhibited apoptotic neuronal death at 24h after reoxygenation.
Our results clearly demonstrated that XXMD is neuroprotective and appears to influence deleterious pathological processes that are activated after the onset of ischemia.
消眩止鸣汤(XXMD)长期以来一直被用于中医治疗中风。
研究 XXMD 在体内和体外中风模型中的神经保护作用及其机制。
采用成年 Wistar 大鼠四血管闭塞和原代培养神经元氧葡萄糖剥夺两种模型,分别模拟体内和体外的缺血再灌注损伤。观察 XXMD 对缺血后海马 CA1 区神经元损伤、caspase-3 活性和 Bcl-2 表达的影响。缺血/再灌注后 7 天,采用 Morris 水迷宫测定认知能力。
XXMD 口服给药可显著增加短暂全脑缺血诱导后第 3 天和第 7 天海马 CA1 区存活神经元的密度,呈剂量依赖性。XXMD 改善了短暂全脑缺血引起的严重空间认知功能障碍。XXMD 可抑制缺血后大鼠 caspase-3 活性的抑制和 Bcl-2 表达的上调。在氧葡萄糖剥夺模型中,XXMD 提取物和高剂量 XXMD 治疗大鼠血液制备的含药血清均可在再氧合后 24 小时抑制凋亡性神经元死亡。
本研究结果清楚地表明,XXMD 具有神经保护作用,并可能影响缺血后激活的有害病理过程。