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浙江大学学报（医学版）
J Zhejiang Univ (Med Sci)  2020, Vol. 49 Issue (5): 623-628    DOI: 10.3785/j.issn.1008-9292.2020.10.12
    
Research progress on macrophage in radiation induced lung injury
LI Mengyao(),LIU Pan,KE Yuehai,ZHANG Xue*()
School of Basic Medical Sciences, Zhejiang University, Hangzhou 310058, China
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Abstract  

Radiation-induced lung injury (RILI), including acute radiation pneumonitis and chronic radiation-induced pulmonary fibrosis (RIPF), is a side effect of radiotherapy for lung cancer and esophageal cancer. Pulmonary macrophages, as a kind of natural immune cells maintaining lung homeostasis, play a key role in the whole pathological process of RILI. In the early stage of RILI, classically activated M1 macrophages secrete proinflammatory cytokines to induce inflammation and produce massive reactive oxygen species (ROS) through ROS-induced cascade to further impair lung tissue. In the later stage of RILI, alternatively activated M2 macrophages secrete profibrotic cytokines to promote the development of RIPF. The roles of macrophage in the pathogenesis of RILI and the related potential clinical applications are summarized in this review.

Key words： Macrophages      Radiation-induced lung injury      Reactive oxygen species      Inflammation      Pulmonary fibrosis      Review     
Received: 03 February 2020      Published: 19 November 2020
CLC:  R818  
Corresponding Authors: ZHANG Xue     E-mail: 21818541@zju.edu.cn;zhangxue@zju.edu.cn
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LI Mengyao
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ZHANG Xue
Cite this article:

LI Mengyao,LIU Pan,KE Yuehai,ZHANG Xue. Research progress on macrophage in radiation induced lung injury. J Zhejiang Univ (Med Sci), 2020, 49(5): 623-628.

URL:

http://www.zjujournals.com/med/10.3785/j.issn.1008-9292.2020.10.12     OR     http://www.zjujournals.com/med/Y2020/V49/I5/623


放射性肺损伤中巨噬细胞作用机制的研究进展

放射性肺损伤（RILI）是肺癌、食管癌等恶性肿瘤患者进行放射治疗时产生的不良反应，包括急性放射性肺炎和慢性放射性肺纤维化。肺巨噬细胞是维持肺部稳态的一种天然免疫细胞，在RILI整个病理过程中均发挥关键作用。在RILI早期，肺巨噬细胞发生M1型活化，分泌炎性细胞因子，诱导炎症反应，同时通过促进活性氧诱导的活性氧级联反应产生大量活性氧，进一步损伤肺组织。在RILI中晚期，肺巨噬细胞向M2型转化，分泌促纤维细胞因子，促进放射性肺纤维化的发展。本文总结了肺巨噬细胞在RILI发病机制中的作用以及潜在的临床应用前景。


关键词： 巨噬细胞,  放射性肺损伤,  活性氧,  炎症,  肺纤维化,  综述 
作用机制 药物 参考文献序号
减轻氧化损伤
  清除氧自由基并维持细胞内超氧化物歧化酶和谷胱甘肽水平 橙皮苷 30
  抑制高速泳动族蛋白B1/Toll样受体4/核因子κB途径 GTS-21 31
  抑制巨噬细胞-NADPH氧化酶-活性氧-肌成纤维细胞轴 雷公藤内酯 32
  抵抗脂质过氧化 褪黑素 33
减轻炎症反应
  调节巨噬细胞促炎编程，抑制M1型活化 鬼臼毒素和芦丁(G-003M) 34
  抑制巨噬细胞中的黑色素瘤缺乏因子炎性小体介导的炎症反应 穿心莲内酯 35
  抑制巨噬细胞浸润 姜黄素 36
  抑制趋化因子配体8表达和巨噬细胞募集 尼卡芬 37
  抑制白细胞介素4-白细胞介素4受体α1-双氧化酶2途径 二甲双胍、褪黑素 38
  抑制微小RNA-30e/NOD样受体家族3途径 褪黑素 38
  抑制巨噬细胞M1型活化及减少炎性细胞因子分泌 2-甲氧基雌二醇 39
抑制纤维化形成
  阻断水通道蛋白4，减少M2型巨噬细胞浸润 TGN-020 40
  抑制高速泳动族蛋白B1及其他促纤维化因子 丙酮酸乙酯 41
  抑制转化生长因子β1-Smad依赖性途径 CpG-寡脱氧核苷酸 42
  减少巨噬细胞浸润和促纤维化因子表达 岩藻依聚糖 43
  抑制过氧化物酶1/核因子κB/缺氧诱导因子1α途径 β-榄香烯 44
减少促炎因子生成和Nrf信号转录，抑制转化生长因子β介导的纤维化 克拉霉素 45
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