A metabolomics study of the inhibitory effect of 17-beta-estradiol on osteoclast proliferation and differentiation.
作者： Xiaoyan Liu , Yanqiu Liu , Mengchun Cheng , Xiaozhe Zhang , Hongbin Xiao
DOI: 10.1039/C4MB00528G
关键词:
摘要: Estradiol is a major drug used clinically to alleviate osteoporosis, partly through inhibition of the activity osteoclasts, which play crucial role in bone resorption. So far, little known about effects estradiol on osteoclast metabolism. In this study, ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC/MS)-based metabolomics strategy was investigate metabolite response 17β-estradiol mouse RAW264.7, commonly cell model for studying osteoporosis. Our results showed that application altered levels 27 intracellular metabolites, including lysophosphatidylcholines (LysoPCs), other lipids and amino acid derivants. The changes all metabolites were observed study induced proliferation (1 μM applied), while only 18 differentiation (0.1 applied). Further pathway impact analysis determined glycerophospholipid metabolism as main potential target estradiol, further confirmed by LCAT (phosphatidylcholine-sterol acyltransferase) lipid peroxidative product (MDA, methane dicarboxylic aldehyde) caused estradiol. Additionally, we found significantly decreased oxidative stress during but not differentiation. suggested generated highly condition-dependent influence
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