Molecular mechanisms of caffeic acid phenethyl esteron blocking deterioration of C6-glioma cells

• Main Authors: Wen -Hai, 梁文海
• Other Authors: Tsui-Hwa Tseng
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/58169849634779600888

碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 96 === Caffeic acid phenethyl ester (CAPE) which is one of component of propolis, has been reported to possess anti-inflammatory, anti-bacterial, anti-virus, hemostasis and anti-tumor activity. Previous, Our laboratory demonstrated the role of MAPKs signal pathway, p53, cytochrome c released and activated caspase-9,caspase-3 in regulating the CAPE(＞50μM)-induced apoptosis in C6-glioma cells. In addition, it demonstrated GFAP, S-100β protein expression mediated blocking cell deterioration by CAPE(＜10μM). However, the signals mediating C6-Glioma apoptosis and blocking deterioration by CAPE(＞50μM, ＜10μM) have not yet been clarified. In the present study, by western blot, HPTLC, DAPI Stain, DNA eletrophoresis, fluorescence spectrograph, Boyden chamber and wound healing assay. We concluded result that CAPE (＞50μM) induced apoptosis of C6-glioma cell through reduction of GSH, activation of SMase/ceramide, activation of p38 Kinase and upregulation of NGF/p75 cascade, JNK Kinase involving ERK activation . Another , CAPE (＜10μM) blocked deterioration of C6 glioma cell through activation of NGF/p75, expression of well differentiated protein (GFAP, S-100β, RhoB) and reduction of (MMP-2,MMP-9) activity. In conclusion, the role of N-SMase/ceramide, MAPKs signal pathway and NGF/p75 in regulating the CAPE (＞50μM) induced apoptosis of C6-glioma cells. In addition, the role of NGF/p75, differentiated protein (GFAP, S-100β, RhoB) and (MMP-2,MMP-9) in regulating the CAPE (＜10μM) blocking deterioration of C6-glioma cells.