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氧化应激在放射性肺损伤中的相关研究进展
引用本文:陈曦,赵路军,徐利明,王平. 氧化应激在放射性肺损伤中的相关研究进展[J]. 中华放射医学与防护杂志, 2016, 36(4): 312-315
作者姓名:陈曦  赵路军  徐利明  王平
作者单位:300060 天津医科大学肿瘤医院放疗科 国家肿瘤临床医学研究中心 天津市肿瘤防治重点实验室,300060 天津医科大学肿瘤医院放疗科 国家肿瘤临床医学研究中心 天津市肿瘤防治重点实验室,300060 天津医科大学肿瘤医院放疗科 国家肿瘤临床医学研究中心 天津市肿瘤防治重点实验室,300060 天津医科大学肿瘤医院放疗科 国家肿瘤临床医学研究中心 天津市肿瘤防治重点实验室
基金项目:国家自然科学基金(30970864)
摘    要:
放射治疗是胸部恶性肿瘤的重要治疗手段。放射性肺损伤是胸部放疗的主要剂量限制因素。射线作用于机体产生大量内源性和外源性活性氧/氮类物质。这些物质通过对DNA、蛋白质及脂膜的直接作用使细胞结构破坏,功能缺失,是早期肺损伤的重要原因。此外,通过一系列细胞、细胞因子的作用,慢性氧化应激逐渐形成,参与细胞通透性增加、组织水肿、细胞外基质纤维蛋白堆积的过程,最终导致放射性纤维化。氧化应激学说为人们更深入地认识放射性肺损伤提供了新的线索和途径,一些抗氧化应激药物也显示了良好的临床应用前景。

关 键 词:氧化应激  放射性肺损伤  活性氧类物质
收稿时间:2015-11-11

Research progress of oxidative stress in radiation-induced lung injury
Chen Xi,Zhao Lujun,Xu Liming and Wang Ping. Research progress of oxidative stress in radiation-induced lung injury[J]. Chinese Journal of Radiological Medicine and Protection, 2016, 36(4): 312-315
Authors:Chen Xi  Zhao Lujun  Xu Liming  Wang Ping
Affiliation:Department of Radiation Oncology, Tianjin Medical University Cancer Institnte and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, Tianjin 300060, China,Department of Radiation Oncology, Tianjin Medical University Cancer Institnte and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, Tianjin 300060, China,Department of Radiation Oncology, Tianjin Medical University Cancer Institnte and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, Tianjin 300060, China and Department of Radiation Oncology, Tianjin Medical University Cancer Institnte and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, Tianjin 300060, China
Abstract:
Although it has been frequently used to treat thoraxic tumors, radiation induced lung injury (RILI) is the major factor of dose limitation in thoracic radiotherapy. Amount of endogenous and exogenous reactive oxygen/nitrogen species (ROS/RNOS) could be generated in the radiated organisms and further cause molecular damage of DNA, protein and membrane lipids, which results in celluar structure damage, dysfunction and RILI. In addition, a series of cytokines could also induce chronic oxidative stresses that contribute to increases in cell membrane permeability, tissue edema and extracellular matrix proteins accumulation and even further result in pulmonary fibrosis. Oxidative stress theory offers new clues and strategies for further understanding the mechanism of RILI, and some anti-oxidative stress drugs may have potential clincial application in RILI treatment.
Keywords:Oxidative stress  Radiation-induced lung injury  Reactive oxygen species
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