Butein up-regulates the expression of the pi class of glutathione S-transferase in rat primary hepatocytes through the ERK/AP-1 pathway

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 健康照護學院 > 營養學系暨碩士班 > 期刊論文 > Item 310903500/28482

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/28482

题名:	Butein up-regulates the expression of the pi class of glutathione S-transferase in rat primary hepatocytes through the ERK/AP-1 pathway
作者:	(Hebron C Chang);陳暉雯(Haw-Wen Chen);(Hui-Shan Tung);(Kai-Li Liu);蔡佳文(Chia-Wen Tsai);李宗貴(Chong-Kuei Lii)
贡献者:	健康照護學院營養學系
关键词:	Butein;π class of glutathione S-transferase;extracellular signal-regulated kinase;activator protein-1;rat primary hepatocytes
日期:	2010-07
上传时间:	2010-09-23 19:57:00 (UTC+8)
摘要:	Induction of phase II enzymes is an important mechanism of chemoprevention. Here we compared the effects of chalcones on the expression of the π class of glutathione S-transferase (GSTP) in rat primary hepatocytes. Hepatocytes were treated with 10 or 25 μM of phloretin or butein for 24 h. Both butein and phloretin dose-dependently increased GSTP protein expression, and the induction potency of butein was stronger than that of phloretin. The increase in GSTP mRNA in cells treated with 25 μM of phloretin and butein was 107% and 211%, respectively (P < 0.05). Butein increased GST enzyme activity by 27% compared with that in the control cells (P < 0.05). In contrast, phloretin had no significant effect on GST enzyme activity. The pTA-luciferase reporter construct with the rat −2.7 kb GSTP promoter region was transiently transfected into Clone 9 liver cells, and the luciferase activity in butein-treated cells was 1.1-fold higher than that in control cells (P < 0.05). GSTP enhancer 1 (GPE1) deletion abolished the induction of reporter activity by butein. The phosphorylation of extracellular signal-regulated kinase (ERK), but not of c-Jun NH2-terminal kinase (JNK) and p38, was stimulated in the presence of butein. Pretreatment with PD98059, an ERK inhibitor, alleviated the increase in activator protein-1 (AP-1)-DNA binding activity and also the activation of GSTP protein expression by butein. Moreover, c-Jun is likely to bind to the GPE1. Silencing of ERK2 by siRNA gene knockdown reduced the butein-induced expression of GSTP. In conclusion, the increased GSTP expression by butein is likely related to the ERK-AP-1 pathway.
關聯:	JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY ():
显示于类别:	[營養學系暨碩士班 ] 期刊論文

文件中的档案:

档案	描述	大小	格式	浏览次数
index.html		0Kb	HTML	393	检视/开启
index.html		0Kb	HTML	484	检视/开启

在CMUR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....