title: An analysis on the suppression of NO and PGE2 by diphenylheptane A and its effect on glycerophospholipids of lipopolysaccharide-induced RAW264.7 cells with UPLC/ESI-QTOF-MS.
abstract: Diarylheptanoid A, 5-hydroxy-7-(4'-hydroxy-3'-methoxyphenyl)-1-phenyl-3-heptanone, is a naturally occurring phytochemical ingredient isolated from the rhizome of Alpinia officinarum. In order to confirm the anti-inflammatory activity of diphenylheptane A, we investigated its effects on lipopolysaccharide (LPS)-induced pro-inflammatory mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2), interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α), as well as upstream genes, including the inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor κB (NF-κB) p65, p38 mitogen-activated protein kinase (MAPK), and extracellular signal-regulated kinase 1/2 (ERK1/2). Our results have proved the anti-inflammatory property of diphenylheptane A. Based on this finding, an LPS-induced RAW264.7 cell inflammatory model was introduced to evaluate the anti-inflammatory activity associated with glycerophospholipid (GPL) metabolism regulated by diphenylheptane A. We applied ultra-performance liquid chromatography/electrospray ionization-quadruple time of flight-mass spectrometry (UPLC/ESI-QTOF-MS) to the metabolic profiling of GPL synthesis in LPS-stimulated macrophages with the aim of identifying differentially synthesized GPL metabolites. Sixteen GPL metabolites, whose changes were restored to normal level after diphenylheptane A treatment, were further screened to be considered as useful biomarkers of inflammation. Overall, our study revealed for the first time that diphenylheptane A reestablished the production of 16 plasma membrane GPLs to basal level in LPS-activated RAW264.7 cells, suggesting the potential therapeutic property of phytochemical compounds against inflammatory diseases.
authors.affiliation: Central Laboratory, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China.
authors.forename: Yuqi
authors.initials: Y
authors.lastname: She
authors.affiliation: Central Laboratory, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China.
authors.forename: Qifan
authors.initials: Q
authors.lastname: Zheng
authors.affiliation: Central Laboratory, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China.
authors.forename: Xuerong
authors.initials: X
authors.lastname: Xiao
authors.affiliation: Central Laboratory, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China. wxiaxia@163.com.
authors.forename: Xia
authors.initials: X
authors.lastname: Wu
authors.affiliation: Central Laboratory, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China. tfengyf@163.com.
authors.forename: Yifan
authors.initials: Y
authors.lastname: Feng
mesh_terms: D000818:Animals; D002460:Cell Line; D002853:Chromatography, Liquid / Q000379:methods*; D015232:Dinoprostone / Q000378:metabolism*; D006536:Heptanes / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D021241:Spectrometry, Mass, Electrospray Ionization / Q000379:methods*
chemical_list: D006536:Heptanes; D009569:Nitric Oxide; D015232:Dinoprostone
keywords: Glycerophospholipid biomarkers; Inflammation; Metabolic profiling; RAW264.7 cells; UPLC/ESI-QTOF-MS