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

被引:7
作者
Chen, Chu-Yue
Jang, Jung-Hee
Park, Mi Hyun
Hwang, Sung Joo
Surh, Young-Joon
Park, Ock Jin
机构
[1] Hannam Univ, Dept Food & Nutr, Taejon 306791, South Korea
[2] Seoul Natl Univ, Coll Pharm, Seoul, South Korea
来源
SIGNAL TRANSDUCTION PATHWAYS, PT C: CELL SIGNALING IN HEALTH AND DISEASE | 2007年 / 1095卷
关键词
Saengshik; neuroprotective effects; antioxidant capacity; PC12; cells; Alzheimer's disease; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; FREE-RADICALS; TOXICITY; HYPOTHESIS; GENES; PRESENILINS; NEURONS; CELLS;
D O I
10.1196/annals.1397.043
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:399 / 411
页数:13
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