文献类型：期刊文献

英文题名：A cellular lipidomic study on the Aβ-induced neurotoxicity and neuroprotective effects of EGCG by using UPLC/MS-based glycerolipids profiling and multivariate analysis

作者：Zhang, Hongyang[1,2];Wang, Jing-Rong[1,3];Yau, Lee Fong[3];Ho, Hing Man[3];Chan, Chi Leung[3];Hu, Ping[2];Liu, Liang[1,3];Jiang, Zhi-Hong[1,3]

机构：[1]Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau Inst Appl Res Med & Hlth, Macau, Peoples R China;[2]E China Univ Sci & Technol, Sch Chem & Mol Engn, Shanghai 200237, Peoples R China;[3]Hong Kong Baptist Univ, Sch Chinese Med, Kowloon Tong, Hong Kong, Peoples R China

年份：2012

卷号：8

期号：12

起止页码：3208

外文期刊名：MOLECULAR BIOSYSTEMS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000311473200010)】；

基金：This study was financially supported by Macao Science and Technology Development Fund, MSAR (039/2011/A2 to ZHJ).

语种：英文

摘要：The aim of this study was to investigate the cellular lipid metabolism associated with beta-amyloid peptide (A beta)-induced neurotoxicity as well as the neuroprotective effect of (-)-epigallocatechin gallate (EGCG), a major polyphenol in green tea. An ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based lipidomic approach was developed to screen and identify changes of the glycerolipids (GL) upon A beta treatment with or without the presence of EGCG in PC12 cells. Principle component analysis (PCA) showed that the A beta-treated group was well separated from the control group, whereas the EGCG group was closer to the control group. The GL levels were significantly elevated in A beta-treated cells compared with the control group, but were restored near to normal levels after EGCG treatment. The elevated phosphatidylcholines (PCs) levels observed in the A beta-treated PC12 cells were quite probably the integrated results of the reduced phospholipase A(2) (PLA(2)) activity and the enhanced activity of lysophospholipid acyltransferases. Moreover, an increased liberation of arachidonic acid (AA) from PCs was observed as another important response of PC12 cells to the A beta aggregates, implying an active inflammatory process occurring in A beta induced neurotoxicity. EGCG treatment can reverse the deregulated metabolism of PCs, which might be one of the biochemical mechanisms contributing to its neuroprotective effect. Collectively, results obtained from the current lipidomic analyses of PC12 cells provided important insight into the biochemical mechanisms underlying A beta-induced neurotoxicity and neuro protective effects of EGCG. This is the first report of the lipidomic study on the neuroprotective effect of EGCG.