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植物提取物(生食)通过抑制线粒体功能障碍和抗氧化作用介导的β-淀粉样蛋白诱导的细胞凋亡的减弱。

Attenuation of Abeta-induced apoptosis of plant extract (Saengshik) mediated by the inhibition of mitochondrial dysfunction and antioxidative effect.

作者信息

Chen Chu-Yue, Jang Jung-Hee, Park Mi Hyun, Hwang Sung Joo, Surh Young-Joon, Park Ock Jin

机构信息

Department of Food and Nutrition, Hannam University, 133 Ojeong-dong Daedeok-gu, Daejeon 306-791, Korea.

出版信息

Ann N Y Acad Sci. 2007 Jan;1095:399-411. doi: 10.1196/annals.1397.043.

Abstract

Recently, considerable attention has been focused on dietary manipulation of oxidative and/or nitrosative damage on neuronal cells. In this article, a neuroprotective effect of plant (Saengshik) extracts was investigated. Rat pheochromocytoma (PC12), cells treated with beta-amyloid underwent apoptotic death as determined by positive in situ terminal end-labeling (TUNEL staining), decreased mitochondrial transmembrane potential, and elevated caspase-3 activity co-occurring with enhanced MDA accumulation and the reduction of GSH levels. Saengshik pretreatment attenuated beta-amyloid-induced apoptosis in PC12 cells possibly by inhibiting mitochondrial dysfunction and exerting antioxidant properties. Saengshik pretreatment inhibited the loss of mitochondrial membrane potentials and reduced the activation of caspase-3. The in vitro antioxidant activities of Saengshik extracts were verified by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) method and superoxide dismutase (SOD) mimetic activity. In beta-amyloid-challenged PC12 cells, Saengshik prevented the production of ROS, decreased the level of MDA, and elevated GSH. The potential of Saengshik as one of the neuroprotective regimens has been suggested through this article, and the combination with defined pharmaceuticals or other dietary antioxidants may provide a better therapeutic or preventive advantage for the management of Alzheimer's disease.

摘要

最近,对神经元细胞氧化和/或亚硝化损伤的饮食调控受到了广泛关注。在本文中,研究了植物(生식)提取物的神经保护作用。用β-淀粉样蛋白处理的大鼠嗜铬细胞瘤(PC12)细胞发生凋亡性死亡,这通过原位末端标记阳性(TUNEL染色)、线粒体跨膜电位降低、caspase-3活性升高以及MDA积累增加和GSH水平降低共同确定。生식预处理可能通过抑制线粒体功能障碍和发挥抗氧化特性来减轻β-淀粉样蛋白诱导的PC12细胞凋亡。生식预处理抑制了线粒体膜电位的丧失并降低了caspase-3的激活。通过1,1-二苯基-2-苦基肼(DPPH)法和超氧化物歧化酶(SOD)模拟活性验证了生식提取物的体外抗氧化活性。在β-淀粉样蛋白攻击的PC12细胞中,生식可防止ROS的产生,降低MDA水平,并提高GSH水平。本文提出了生식作为神经保护方案之一的潜力,并且与特定药物或其他膳食抗氧化剂联合使用可能为阿尔茨海默病的治疗或预防提供更好的优势。

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