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低剂量放射治疗炎症性疾病中的放射生物学机制。

Radiobiological mechanisms in inflammatory diseases of low-dose radiation therapy.

作者信息

Rödel F, Keilholz L, Herrmann M, Sauer R, Hildebrandt G

机构信息

Department of Radiotherapy, University of Erlangen-Nuremberg, Erlangen, Germany.

出版信息

Int J Radiat Biol. 2007 Jun;83(6):357-66. doi: 10.1080/09553000701317358.

DOI:10.1080/09553000701317358
PMID:17487675
Abstract

PURPOSE

Whereas X-irradiation with high doses is established to exert pro-inflammatory effects, low-dose radiotherapy (LD-RT) with single fractions below 1.0 Gy and a total dose below 12 Gy is clinically well known to exert anti-inflammatory and analgesic effects on several inflammatory diseases and painful degenerative disorders. Experimental studies to confirm the effectiveness, the empirical dose and fractionation schemes, and the underlying radiobiological mechanisms are still fragmentary.

METHOD

The anti-inflammatory efficiency of LD-RT was confirmed in several experimental in vitro and in vivo models.

RESULTS

In vitro studies revealed a variety of mechanisms related to the anti-inflammatory effect, in particular the modulation of cytokine and adhesion molecule expression on activated endothelial cells and leukocytes, and of nitric oxide (NO) production and oxidative burst in activated macrophages and native granulocytes.

CONCLUSION

Inflammatory diseases are the result of complex and pathologically unbalanced multicellular interactions. It is, therefore, reasonable to assume that further molecular pathways and cellular components contribute to the anti-inflammatory effect of LD-RT. This review discusses data and models revealing aspects of the mechanisms underlying the anti-inflammation induced by low doses of X-irradiation and may serve as a basis for systematic analyses, necessary to optimize LD-RT in clinical practice.

摘要

目的

鉴于高剂量X射线辐射具有促炎作用,临床已熟知单次剂量低于1.0 Gy且总剂量低于12 Gy的低剂量放疗(LD-RT)对多种炎症性疾病和疼痛性退行性疾病具有抗炎和镇痛作用。然而,用于证实其有效性、经验性剂量和分割方案以及潜在放射生物学机制的实验研究仍然不完整。

方法

在多个体外和体内实验模型中证实了LD-RT的抗炎效果。

结果

体外研究揭示了多种与抗炎作用相关的机制,特别是对活化内皮细胞和白细胞上细胞因子和黏附分子表达的调节,以及对活化巨噬细胞和天然粒细胞中一氧化氮(NO)产生和氧化爆发的调节。

结论

炎症性疾病是复杂且病理上失衡的多细胞相互作用的结果。因此,有理由推测还有其他分子途径和细胞成分参与LD-RT的抗炎作用。本综述讨论了揭示低剂量X射线辐射诱导抗炎作用机制方面的数据和模型,可为临床实践中优化LD-RT所需的系统分析提供依据。

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