English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 6507/11669
造訪人次 : 30040482      線上人數 : 629
RC Version 3.2 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 進階搜尋

請使用永久網址來引用或連結此文件: http://ir.ncue.edu.tw/ir/handle/987654321/14956

題名: Involvement of Tumor Suppressor Protein p53 and p38 MAPK in Caffeic Acid Phenethyl Ester-induced Apoptosis of C6 Glioma Cells
作者: Lee, Yean-Jang;Kuo, H. C.;Wang, C. J.;Lee, M. J.;Lin, W. C.;Tseng, T. H.
貢獻者: 化學系
日期: 2003-12
上傳時間: 2012-12-10T02:51:50Z
出版者: Elsevier
摘要: Caffeic acid phenethyl ester (CAPE), an active component of propolis, has many biological and pharmacological activities including antioxidant, anti-inflammation, antiviral action, and anticancer effect. Our previous studies showed that CAPE exhibited significant cytotoxicity in oral cancer cells. Herein we further investigated the cytotoxicity potential of CAPE and the mechanism of its action in C6 glioma cells. The data exhibited that C6 glioma cells underwent internucleosomal DNA fragmentation 24 hr after the treatment of CAPE (50 microM). The proportion of C6 glioma cells with hypodiploid nuclei was increased to 24% at 36 hr after the exposure. Further results showed that CAPE induced the release of cytochrome c from mitochondria into cytosol, and the activation of CPP32. CAPE application also enhanced the expression of p53, Bax, and Bak. Finally, the potential signaling components underlying CAPE induction of apoptosis were elucidated. We found that CAPE activated extracellular signal-regulated kinase (ERKs) and p38 mitogen-activated protein kinase (p38 MAPK) in C6 glioma cells. More importantly, p38 kinase formed a complex with p53 after the treatment of CAPE for 0.5 hr. The expression of p53, phospho-serine 15 of p53, and Bax, and inactivate form of CPP32 was suppressed by a pretreatment of a specific p38 MAPK inhibitor, SB203580. The resultant data suggest that p38 MAPK mediated the CAPE-induced p53-dependent apoptosis in C6 glioma cells.
關聯: Biochemical Pharmacology, 66(12): 2281-2289
顯示於類別:[化學系] 期刊論文

文件中的檔案:

檔案 大小格式瀏覽次數
index.html0KbHTML664檢視/開啟


在NCUEIR中所有的資料項目都受到原著作權保護.

 


DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回饋