Vitamin D receptor mediates liver ischemia and reperfusion injury by autophagy-regulated M2 macrophage polarization.

Mingming Fang, Chen Zhong
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Abstract

Liver ischemia and reperfusion (IR) injury is the major complication of liver-related operations. Macrophage polarization has an essential effect on the mechanism of liver IR injury. Vitamin D receptor (VDR) has been found to regulate macrophage polarization and alleviate IR injury. Nevertheless, the correlation between VDR and macrophage polarization in liver IR injury has not been clearly elucidated. VDR knockout mice and wild-type littermates underwent partial liver ischemia for 90 min and reperfusion for 6 h. RAW264.7 cells were also used to verify the influence of VDR on macrophage polarization in vitro. VDR activation could promote M2 macrophage polarization and then reduce liver injury. In contrast, VDR deficiency aggravated the liver injury by disturbing M2 macrophage polarization. Moreover, autophagy participated in the effect of VDR on M2 macrophage polarization through mediating suppressor of cytokine signaling. Therefore, VDR plays a vital influence in liver IR injury. The protective role of VDR activation in liver IR injury is related to regulate M2 macrophage polarization by autophagy.

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维生素D受体通过自噬调节的M2巨噬细胞极化介导肝脏缺血再灌注损伤。
肝脏缺血再灌注损伤是肝脏相关手术的主要并发症。巨噬细胞极化在肝脏IR损伤机制中起重要作用。维生素D受体(VDR)具有调节巨噬细胞极化和减轻IR损伤的作用。然而,肝IR损伤中VDR与巨噬细胞极化的相关性尚未明确。VDR基因敲除小鼠和野生型幼崽肝脏局部缺血90 min,再灌注6 h,并采用RAW264.7细胞体外验证VDR对巨噬细胞极化的影响。激活VDR可促进M2巨噬细胞极化,减轻肝损伤。相反,VDR缺乏通过扰乱M2巨噬细胞极化加重肝损伤。此外,自噬通过介导细胞因子信号的抑制参与了VDR对M2巨噬细胞极化的影响。因此,VDR在肝脏IR损伤中起着至关重要的作用。激活VDR对肝脏IR损伤的保护作用与通过自噬调节M2巨噬细胞极化有关。
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