title: Propofol inhibits hypoxia/reoxygenation-induced human gastric epithelial cell injury by suppressing the Toll-like receptor 4 pathway.
abstract: This study aimed to investigate the role of the Toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under hypoxia/reoxygenation (H/R) in vitro, and the effect of propofol on injured GES-1 cells as well as its possible mechanism. Before H/R induction, GES-1 cells were preconditioned with fat emulsion, propofol, or epigallocatechin gallate. Then cell viability, cell apoptosis, and related molecules in the cells were analyzed under experimental conditions. We found that propofol 50 μmol/L markedly inhibited the H/R injury under hypoxia 1.5 h/reoxygenation 2 hours by promoting GES-1 cell viability and decreasing cell apoptosis. The TLR4 signal may be involved in the protective effect of propofol against H/R injury. The malondialdehyde contents and superoxide dismutase activities were recovered under propofol preconditioning. In summary, propofol preconditioning may exert a protective effect on H/R injury in GES-1 cells and the mechanism may be via inhibition of the activated TLR4 signal under H/R conditions.
authors.affiliation: Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou, China.
authors.forename: Jiao-Li
authors.initials: JL
authors.lastname: Zhang
authors.forename: Su-Juan
authors.initials: SJ
authors.lastname: Fei
authors.forename: Xia
authors.initials: X
authors.lastname: Qin
authors.forename: Hui-Hui
authors.initials: HH
authors.lastname: Ye
authors.forename: He-Xia
authors.initials: HX
authors.lastname: Liu
authors.forename: Xiao-Jing
authors.initials: XJ
authors.lastname: Dai
authors.forename: Yong-Mei
authors.initials: YM
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D015687:Cell Hypoxia / Q000187:drug effects / Q000235:genetics; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D004847:Epithelial Cells / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology*; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D009336:Necrosis; D010100:Oxygen / Q000494:pharmacology*; D015742:Propofol / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics; D013482:Superoxide Dismutase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D020672:I-kappa B Proteins; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; C000606204:NFKBIA protein, human; D012333:RNA, Messenger; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D051996:Transcription Factor RelA; D051028:bcl-2-Associated X Protein; D000072000:NF-KappaB Inhibitor alpha; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D010100:Oxygen; D015742:Propofol