Park Yong-Hoon, Son Il Hong, Kim Bokyung, Lyu Yeoung-Su, Moon Hyung-In, Kang Hyung-Won
INAM Neuroscience Research Center, Sanbon Medical Center, Wonkwang University, South Korea.
Pharmazie. 2009 Nov;64(11):760-4.
Beta-amyloid (Abeta)-induced neurotoxicity is considered to be mediated through the formation of reactive oxygen species (ROS). In this study, the protective effects of Poria cocos water extract (PCW) against Abeta1-42-induced cell death were investigated using rat pheochromocytoma (PC12) cells. Exposure of PC12 cells to the Abeta1-42 (20 microM) for 48h resulted in neuronal cell death, whereas pretreatment with PCW at the concentration range of 5-125 microg/ml reduced Abeta1-42-induced cell death. In addition, PC12 cells treated with Abeta1-42 exhibited increased accumulation of intracellular oxidative damages and underwent apoptotic death as determined by characteristic morphological alterations and positive in situ terminal end-labeling (TUNEL staining). However, PCW attenuated Abeta1-42-induced cytotoxicity, apoptotic features, and accumulation of intracellular oxidative damage. Moreover, PCW (5 to 125 microg/ml) decreased expression of apoptotic protein Bax and activity of caspase-3, but enhanced expression of anti-apoptotic protein Bcl-2. These results suggest that PCW may protect cells through suppressing the oxidative stress and the apoptosis induced by Abeta1-42, implying that PCW may be potential natural agents for Alzheimer's diseases.
β-淀粉样蛋白(Aβ)诱导的神经毒性被认为是通过活性氧(ROS)的形成介导的。在本研究中,使用大鼠嗜铬细胞瘤(PC12)细胞研究了茯苓水提取物(PCW)对Aβ1-42诱导的细胞死亡的保护作用。将PC12细胞暴露于Aβ1-42(20μM)48小时导致神经元细胞死亡,而用浓度范围为5-125μg/ml的PCW预处理可减少Aβ1-42诱导的细胞死亡。此外,用Aβ1-42处理的PC12细胞表现出细胞内氧化损伤积累增加,并通过特征性形态学改变和原位末端标记阳性(TUNEL染色)确定发生凋亡死亡。然而,PCW减轻了Aβ1-42诱导的细胞毒性、凋亡特征和细胞内氧化损伤的积累。此外,PCW(5至125μg/ml)降低了凋亡蛋白Bax的表达和caspase-3的活性,但增强了抗凋亡蛋白Bcl-2的表达。这些结果表明,PCW可能通过抑制Aβ1-42诱导的氧化应激和凋亡来保护细胞,这意味着PCW可能是治疗阿尔茨海默病的潜在天然药物。