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• W1860141269 startingPage "1565" @default.
• W1860141269 abstract "Severe acute liver injury due to accidental or intentional acetaminophen overdose presents a major clinical dilemma often requiring liver transplantation. In the present study, liver regeneration after profound liver injury in mice challenged with acetaminophen was facilitated by the exogenous addition of ELR-containing CXC chemokines such as macrophage inflammatory protein-2 (MIP-2), epithelial neutrophil-activating protein-78 (ENA-78), or interleukin 8. Intravenous administration of ELR-CXC chemokines or N-acetyl-cysteine (NAC) immediately after acetaminophen challenge in mice significantly reduced histological and biochemical markers of hepatic injury. However, when the intervention was delayed until 10 h after acetaminophen challenge, only ELR-CXC chemokines significantly reduced liver injury and mouse mortality. The delayed addition of ELR-CXC chemokines to cultured hepatocytes maintained the proliferation of these cells in a CXCR2-dependent fashion after acetaminophen challenge whereas delayed NAC treatment did not. These observations demonstrate that ELR-CXC chemokines represent novel hepatic regenerative factors that exhibit prolonged therapeutic effects after acetaminophen-induced hepatotoxicity." @default.
• W1860141269 created "2016-06-24" @default.
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• W1860141269 date "1999-09-01" @default.
• W1860141269 modified "2023-10-17" @default.
• W1860141269 title "Novel CXCR2‐dependent liver regenerative qualities of ELR‐containing CXC chemokines" @default.
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• W1860141269 doi "https://doi.org/10.1096/fasebj.13.12.1565" @default.
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