Nitric oxide induces prion protein via MEK and p38 MAPK signaling

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 醫學系 > 期刊論文 > Item 310903500/30424

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题名:	Nitric oxide induces prion protein via MEK and p38 MAPK signaling
作者:	Wang, VC;Chuang, TC;Hsu, YD;Chou, WY;Kao, MC
贡献者:	醫學院醫學系生化學科;Natl Def Med Ctr, Dept Biochem, Taipei, Taiwan;China Med Univ, Coll Med, Dept Biochem, Taichung, Taiwan;Tri Serv Gen Hosp, Dept Neurol, Taipei, Taiwan;Tamkang Univ, Dept Chem, Taipei, Taiwan;Natl Def Univ, Natl Def Med Ctr, Grad Inst Med Sci, Taipei, Taiwan;Cardinal Tien Hosp, Dept Neurol, Taipei, Taiwan
日期:	2005
上传时间:	2010-09-24 14:55:09 (UTC+8)
出版者:	ACADEMIC PRESS INC ELSEVIER SCIENCE
摘要:	It has been reported that (-)Menthol can inhibit the growth of rat liver epithelial tumor cells and is a potent chemopreventive agent. The purpose of the present experiment was to examine and identify cellular processes leading to cell death which are affected by (-)Menthol in human gastric SNU-5 cancer cells.. Cell death (cytotoxicity) was examined and analyzed by trypan blue stain and flow cytometric methods. It was shown that (-)Menthol inhibited the proliferation of the cells in a dose- and time-dependent manner, inhibited topoisomerase I, II alpha and II beta, but promoted the levels of NF-kappa B gene expression based on the Western blot and polymerase chain reaction (PCR) and cDNA microarray methods. These data suggest that (-)Menthol may induce cytotoxicity through inhibiting gene expression of topoisomerase I, II alpha a and II beta and promoting the gene expression of NF-kappa B in SNU-5 cells.
關聯:	BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 333(1):95-100
显示于类别:	[醫學系] 期刊論文

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