title: Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells.
abstract: Monocyte chemoattractant protein-1 (MCP-1) is a cytokine that mediates the influx of cells to sites of inflammation. Our group recently reported that propofol exerted an anti-inflammatory effect and could inhibit lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines. However, the effect and possible mechanisms of propofol on MCP-1 expression remain unclear. LPS-stimulated HepG2 cells were treated with 50 μM propofol for 0, 6, 12, and 24 h, respectively. The transcript and protein levels were measured by real-time quantitative PCR and Western blot analyses, respectively. We found that propofol markedly decreased both MCP-1 messenger RNA (mRNA) and protein levels in LPS-stimulated HepG2 cells in a time-dependent manner. Expression of apolipoprotein M (apoM) and forkhead box protein A2 (foxa2) was increased by propofol treatment in HepG2 cells. In addition, the inhibitory effect of propofol on MCP-1 expression was significantly abolished by small interfering RNA against apoM and foxa2 in LPS-stimulated HepG2 cells. Propofol attenuates LPS-induced MCP-1 production through enhancing apoM and foxa2 expression in HepG2 cells.
authors.affiliation: Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Ma
authors.forename: Jia-Yi
authors.initials: JY
authors.lastname: Zhao
authors.forename: Zhen-Long
authors.initials: ZL
authors.lastname: Zhao
authors.forename: Jing
authors.initials: J
authors.lastname: Ye
authors.forename: Shu-Fen
authors.initials: SF
authors.lastname: Li
authors.forename: Hai-Hong
authors.initials: HH
authors.lastname: Fang
authors.forename: Miao-Ning
authors.initials: MN
authors.lastname: Gu
authors.forename: Yan-Wei
authors.initials: YW
authors.lastname: Hu
authors.forename: Zai-Sheng
authors.initials: ZS
authors.lastname: Qin
mesh_terms: D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001053:Apolipoproteins / Q000096:biosynthesis* / Q000235:genetics; D000075243:Apolipoproteins M; D002460:Cell Line; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D056945:Hep G2 Cells; D051542:Hepatocyte Nuclear Factor 3-beta / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D054834:Lipocalins / Q000096:biosynthesis* / Q000235:genetics; D008070:Lipopolysaccharides; D015742:Propofol / Q000494:pharmacology*; D034622:RNA Interference; D012333:RNA, Messenger / Q000096:biosynthesis; D034741:RNA, Small Interfering
chemical_list: C400523:APOM protein, human; D018686:Anesthetics, Intravenous; D000893:Anti-Inflammatory Agents; D001053:Apolipoproteins; D000075243:Apolipoproteins M; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C496502:FOXA2 protein, human; D054834:Lipocalins; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D051542:Hepatocyte Nuclear Factor 3-beta; D015742:Propofol