作者: Tomoharu Yokooji , Teruo Murakami , Ryoko Yumoto , Junya Nagai , Mikihisa Takano
DOI: 10.1016/J.EJPHAR.2006.06.079
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摘要: Abstract The function of multidrug resistance-associated protein 2 (Mrp2) in the intestine and liver, as well intestinal Mrp2 expression, was analyzed CCl4-induced acute hepatic failure rats with hyperbilirubinemia. plasma level bilirubin glucuronides, endogenous Mrp2-substrates, 26 μM at 24 h after CCl4 treatment. levels jejunum decreased to 41% control level. Mrp2-mediated efflux 2,4-dinitrophenyl-S-glutathione (DNP-GSH), an Mrp2-substrate, 31% vitro, almost completely suppressed vivo same that presence probenecid, Mrp2-inhibitor. Biliary excretion DNP-GSH inhibited by intravenous probenecid. suppression increased glucuronides recovered within thereafter. These results suggest hyperbilirubinemia disease states may be related systemic function.