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首页> 外文期刊>Hepatology research: the official journal of the Japan Society of Hepatology >Inhibition of the CXCL12/CXCR4 chemokine axis with AMD3100, a CXCR4 small molecule inhibitor, worsens murine hepatic injury
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Inhibition of the CXCL12/CXCR4 chemokine axis with AMD3100, a CXCR4 small molecule inhibitor, worsens murine hepatic injury

机译：抑制趋化因子CXCL12 / CXCR4轴AMD3100,趋化因子受体CXCR4小分子抑制剂,恶化小鼠肝脏损伤

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摘要

AimActivation of hepatic stellate cells and development of chronic inflammation are two key features in the progression of hepatic fibrosis. We have shown that in vitro activated stellate cells increase their expression of CXCL12 as well as the receptor CXCR4 and that receptor engagement promotes a profibrogenic phenotype. Furthermore, injury promotes increased hepatic expression of CXCL12 and a massive infiltration of CXCR4-expressing leukocytes, granulocytes and myeloid cells. The primary site of inflammatory cell accumulation is around the CXCL12-rich portal tracts and within fibrotic septae, indicating a role for CXCR4 during injury. In order to characterize the relevance of the CXCR4/CXCL12 chemokine axis during hepatic injury we inhibited the axis using AMD3100, a CXCR4 small molecule inhibitor, in models of chronic and acute liver injury.
机译：肝星状细胞和AimActivation慢性炎症是两个重要的发展肝纤维化的进展。我们已经表明,体外活化的肝星状细胞增加CXCL12的表达式随着受体CXCR4受体参与促进profibrogenic表型。此外,肝损伤促进增加CXCL12和大规模渗透的表情CXCR4-expressing白细胞、粒细胞和骨髓细胞。在CXCL12-rich细胞积累门管区纤维化septae,表示一种角色趋化因子受体CXCR4在受伤。为了描述的相关性趋化因子受体CXCR4 / CXCL12趋化因子轴在肝脏损伤我们使用AMD3100抑制轴,趋化因子受体CXCR4小分子抑制剂,在慢性模型和急性肝损伤。

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