ACTIVATION OF PEROXISOME PROLIFERATOR- ACTIVATED RECEPTOR α MODIFIES Aβ-INDUCED NEUROTOXICITY IN HUMAN NT2N CELLS

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 醫學系 > 會議論文 > Item 310903500/21487

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题名:	ACTIVATION OF PEROXISOME PROLIFERATOR- ACTIVATED RECEPTOR α MODIFIES Aβ-INDUCED NEUROTOXICITY IN HUMAN NT2N CELLS
作者:	(Nai-Wen Chang);陳緋娜(Fei-Na Chen);(Jia-Hao Chang);(Pei-Yi Chen1)
贡献者:	醫學院醫學系學士班社會醫學科
日期:	2006-03-18
上传时间:	2009-09-07 11:04:22 (UTC+8)
摘要:	Amyloid-β-peptide (Aβ) deposition within the brains of Alzheimer’s disease (AD) patients results in the neurodegeneration. The peroxisome proliferator-activated receptor α (PPARα) is a lipid activated transcription factor, which controls the promoters of multiple genes encoding enzymes in the lipid metabolic pathways. Recent studies showed that the PPARαL162V polymorphism increased the risk of AD. In this study we determined the effect of activation of PPARα by Wy14643 on Aβ42-induced NT2N (NTera2 neurons) neurotoxicity. We found that the proportion of NT2N cells at Sub-G1 phase increased significantly in the Aβ42+Wy14643 group, compared to Aβ42 group after 24 hours of treatment. As to the extent of apoptosis, caspase 3 protein level, pGsk-3β/Gsk-3β ratio, and Bcl-2/Bax ratio were not significantly different between the Aβ42 group and the Aβ42+Wy14643 group. However, the addition of Wy14643 plus Aβ42 significantly increased the expression of endonuclease G (Endo G) protein, compared to the Aβ42 group. These results suggested that activation of PPARα did not influence the expression of caspase 3 protein, but significantly induced the expression of Endo G protein which accelerated the apoptosis of NT2N cells.
關聯:	台灣生物化學及分子生物學學會
显示于类别:	[醫學系] 會議論文

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