Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea.
J Ethnopharmacol. 2010 Aug 9;130(3):625-30. doi: 10.1016/j.jep.2010.05.040. Epub 2010 Jun 9.
Samjunghwan (SJH) is a multi-herbal traditional medicine composed of Mori Fructus, Lycii Radicis Cortex, and Atractylodis Rhizoma Alba and it is clinically applied as an anti-aging agent in neurodegenerative disorders, to promote longevity. In the present study, we evaluated the neuroprotective effect of SJH in Alzheimer's disease induced by amyloid-beta (Abeta) and examined the related pathways.
To evaluate the protective effect of SJH, we conducted thiazolyl blue tetrazolium bromide, lactate dehydrogenase, and MAP-2 staining assays of primary cultured rat cortical neurons stressed by Abeta(25-35). To investigate the possible mechanism of action, we examined the Bcl-2/Bax expression ratio, mitochondrial membrane potential (Deltapsi(M)), cytochrome C release, and caspase-3 activation, focusing on the mitochondria-mediated apoptotic pathways.
SJH at concentrations of 10 and 100 microg/ml provided significant protection of rat cortical neurons from Abeta(25-35) neurotoxicity. At the maximum effective dose of 100 microg/ml, SJH significantly increased the anti-apoptotic protein (Bcl-2)/pro-apoptotic protein (Bax) ratio and inhibited Deltapsi(M) depolarization, cytosolic cytochrome C release, and caspase-3 activation.
SJH appears to provide neuroprotection against mitochondria-mediated apoptotic pathways in this Abeta(25-35)-induced Alzheimer's disease model.
山茱萸(SJH)是一种由山茱萸、枸杞皮和白术组成的多草药传统药物,临床上用于治疗神经退行性疾病的抗衰老药物,以促进长寿。本研究评估了 SJH 对淀粉样蛋白-β(Abeta)诱导的阿尔茨海默病的神经保护作用,并探讨了相关途径。
为了评估 SJH 的保护作用,我们对 Abeta(25-35)应激的原代培养大鼠皮质神经元进行噻唑蓝溴化四唑、乳酸脱氢酶和 MAP-2 染色检测。为了探讨可能的作用机制,我们检测了 Bcl-2/Bax 表达比、线粒体膜电位(Deltapsi(M))、细胞色素 C 释放和 caspase-3 激活,重点关注线粒体介导的凋亡途径。
SJH 在 10 和 100 μg/ml 浓度下可显著保护大鼠皮质神经元免受 Abeta(25-35)神经毒性的影响。在最大有效剂量 100 μg/ml 时,SJH 显著增加了抗凋亡蛋白(Bcl-2)/促凋亡蛋白(Bax)比值,并抑制了 Deltapsi(M)去极化、细胞溶质细胞色素 C 释放和 caspase-3 激活。
SJH 似乎对 Abeta(25-35)诱导的阿尔茨海默病模型中涉及线粒体的凋亡途径提供了神经保护作用。