Neuroprotective Effect of Luteolin on Amyloid β Protein (25-35)-Induced Toxicity in Cultured Rat Cortical Neurons

被引:61
作者
Cheng, Hao-Yuan [1 ]
Hsieh, Ming-Tsuen [1 ]
Tsai, Fan-Shiu [1 ]
Wu, Chi-Rei [1 ]
Chiu, Chuan-Sung [1 ,2 ]
Lee, Min-Min [3 ]
Xu, Hong-Xi [4 ]
Zhao, Zhong-Zhen [5 ]
Peng, Wen-Huang [1 ]
机构
[1] China Med Univ, Grad Inst Chinese Pharmaceut Sci, Coll Pharm, Taichung, Taiwan
[2] Hsin Sheng Coll Med Care & Management, Pingzhen City 324, Taoyuan County, Taiwan
[3] Asia Univ, Dept Hlth & Nutr Biotechnol, Wufeng 41354, Taichung County, Taiwan
[4] Hong Kong Jockey Club Inst Chinese Med, Chinese Med Lab, Hong Kong, Hong Kong, Peoples R China
[5] Hong Kong Baptist Univ, Sch Chinese Med, Kowloon Tong, Hong Kong, Peoples R China
关键词
luteolin; A beta; cortical neurons; MAP kinases; caspase; 3; SIGMA-RECEPTOR LIGANDS; IN-VITRO; ALZHEIMERS-DISEASE; DOWN-REGULATION; NMDA RECEPTORS; APOPTOSIS; KINASE; INHIBITION; ESTROGEN; FLAVONOIDS;
D O I
10.1002/ptr.2940
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The present study was carried out to investigate the neuroprotective effect of luteolin on amyloid beta (A beta) (25-35)-induced neurotoxicity using cultured rat cortical neurons. After exposure of primary cultures of rat cortical cells to 10 mu M A beta (25-35) for 48 h, cortical cell cultures exhibited marked apoptotic death. Pretreatment with luteolin (1, 10 mu M) significantly protected cortical cell cultures against A beta (25-35)-induced toxicity. Luteolin (1, 10 mu M) showed a concentration-dependent inhibition on 10 mu M Ab (25-35)-induced apoptotic neuronal death, as assessed by MTT assay. Furthermore, luteolin reduced apoptotic characteristics by DAPI staining. For Western blot analysis, the results showed that the protective effect of luteolin on A beta (25-35)-induced neurotoxicity was mediated by preventing of ERK-p, JNK, JNK-p, P38-p and caspase 3 activations in rat primary cortical cultures. Taken together, the results suggest that luteolin prevents A beta (25-35)-induced apoptotic neuronal death through inhibiting the protein level of JNK, ERK and p38 MAP kinases and caspase 3 activations. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:S102 / S108
页数:7
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