Toll-Like Receptor-4 Antagonist (+)-Naltrexone Protects Against Carbamyl-Platelet Activating Factor (cPAF)-Induced Preterm Labor in Mice
Toll样受体-4拮抗剂( ) -Naltrexone对羧甲基-血小板激活因子( cPAF )诱导的小鼠早产有保护作用
作者: Hanan H. WahidPeck Yin ChinDavid J. SharkeyKerrilyn R. DienerMark R. HutchinsonKenner C. RiceLachlan M. MoldenhauerSarah A. Robertson
作者单位: 1Robinson Research Institute and Adelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia
2School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia, Australia
3Australian Research Council Centre of Excellence for Nanoscale BioPhotonics, Adelaide, South Australia, Australia
4Drug Design and Synthesis Section, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, Maryland
刊名: The American Journal of Pathology, 2020, Vol.190 (5), pp.1030-1045
来源数据库: Elsevier Journal
DOI: 10.1016/j.ajpath.2020.01.008
英文摘要: Spontaneous preterm labor is frequently caused by an inflammatory response in the gestational tissues elicited by either infectious or sterile agents. In sterile preterm labor, the key regulators of inflammation are not identified, but platelet-activating factor (PAF) is implicated as a potential rate-limiting effector agent. Since Toll-like receptor (TLR)-4 can amplify PAF signaling, we evaluated whether TLR4 contributes to inflammation and fetal loss in a mouse model of PAF-induced sterile preterm labor, and whether a small-molecule TLR4 inhibitor, (+)-naltrexone, can mitigate adverse PAF-induced effects. The administration of carbamyl (c)-PAF caused preterm labor and fetal loss in wild-type mice but not in TLR4-deficient mice. Treatment with (+)-naltrexone prevented preterm delivery...
全文获取路径: Elsevier  (合作)
影响因子:4.522 (2012)