氧化应激
炎症
巨噬细胞极化
心脏毒性
基因剔除小鼠
医学
药理学
巨噬细胞
阿霉素
免疫学
内分泌学
内科学
化学
受体
毒性
化疗
生物化学
体外
作者
Yanqin Feng,Qingwei Ji,Di Ye,Heng Pan,Xiyi Lu,Liren Gan,Menglong Wang,Jianfang Liu,Yao Xu,Jishou Zhang,Mengmeng Zhao,Shou-Xi Xu,Zheng Yin,Wei Pan,Cheng Wei,Meilin Liu,Jun Wan,Jing Ye
标识
DOI:10.1016/j.bcp.2023.115469
摘要
Several interleukins (ILs) have been demonstrated to participate in cardiac injury. This study aimed to investigate whether IL-27p28 plays a regulatory role in doxorubicin (DOX)-induced cardiac injury by regulating inflammation and oxidative stress.Dox was used to establish a mouse cardiac injury model, and IL-27p28 was knocked out to observe its role in cardiac injury. In addition, monocytes were adoptively transferred to clarify whether monocyte-macrophages mediate the regulatory role of IL-27p28 in DOX-induced cardiac injury.IL-27p28 knockout significantly aggravated DOX-induced cardiac injury and cardiac dysfunction. IL-27p28 knockout also upregulated the phosphorylation levels of p65 and STAT1 and promoted M1 macrophage polarization in DOX-treated mice, which increased cardiac inflammation and oxidative stress. Moreover, IL-27p28-knockout mice that were adoptively transferred WT monocytes exhibited worse cardiac injury and cardiac dysfunction and higher cardiac inflammation and oxidative stress.IL-27p28 knockdown aggravates DOX-induced cardiac injury by worsening the M1 macrophage/M2 macrophage imbalance and its associated inflammatory response and oxidative stress.
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