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首页> 外文期刊>International Journal of Radiation Oncology, Biology, Physics >Anti-inflammatory effects of low-dose radiotherapy in an experimental model of systemic inflammation in mice.
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Anti-inflammatory effects of low-dose radiotherapy in an experimental model of systemic inflammation in mice.

机译：低剂量放疗在小鼠全身性炎症实验模型中的抗炎作用。

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PURPOSE: The aim of this study was to determine the effects of low-dose radiotherapy (LD-RT) on the inflammatory response and to characterize the potential mechanisms underlying these effects. METHODS AND MATERIALS: Mice were irradiated with 0.1, 0.3, 0.6 Gy, or sham radiation before lipopolysaccharide (LPS) challenge. Leukocyte-endothelial cell interactions in intestinal venules were assessed using intravital microscopy. Intercellular adhesion molecule-1 (ICAM-1) expression was determined using radiolabeled antibodies 5 h after irradiation. Production of transforming growth factor-beta1 (TGF-beta1) was measured by enzyme-linked immunosorbent assay and its in vivo functional relevance by immunoneutralization. RESULTS: Compared with vehicle treated animals, LPS induced a marked increase in leukocyte adhesion (0.13+/-0.59 vs. 5.89+/-1.03, p<0.0001) in intestinal venules. The number of adherent leukocytes was significantly reduced by the 3 doses of LD-RT tested; the highest inhibition was observed with 0.3 Gy (0.66+/-1.96, p<0.0001). LPS-induced ICAM-1 upregulation was not modified by LD-RT. Circulating levels of TGF-beta1 were significantly increased in response to LD-RT in controls and LPS challenged animals. Neutralization of TGF-beta1 partially restored LPS-induced adhesion (4.83+/-1.41, p<0.05). CONCLUSIONS: LD-RT has a significant anti-inflammatory effect, inhibiting leukocyte recruitment, which is maximal at 0.3 Gy. This effect results in part from increased TGF-beta1 production and is not related to modulation of ICAM-1 expression.
机译：目的：本研究的目的是确定低剂量放射疗法（LD-RT）对炎症反应的影响并确定潜在的潜在机制。方法和材料：在脂多糖（LPS）攻击之前，先对小鼠进行0.1、0.3、0.6 Gy或假放射线照射。使用活体显微镜检查评估肠道小静脉中白细胞-内皮细胞的相互作用。照射后5小时，用放射性标记的抗体测定细胞间粘附分子-1（ICAM-1）的表达。通过酶联免疫吸附测定法测定转化生长因子β1（TGF-β1）的产生，并通过免疫中和测定其体内功能相关性。结果：与赋形剂处理的动物相比，LPS诱导了肠小静脉白细胞粘附的显着增加（0.13 +/- 0.59对5.89 +/- 1.03，p <0.0001）。 3剂量的LD-RT可以显着减少粘附白细胞的数量。在0.3 Gy（0.66 +/- 1.96，p <0.0001）时观察到最高的抑制作用。 LPS不能改变LPS诱导的ICAM-1上调。在对照组和LPS攻击动物中，对LD-RT的响应，TGF-beta1的循环水平显着增加。 TGF-beta1的中和部分恢复了LPS诱导的粘附（4.83 +/- 1.41，p <0.05）。结论：LD-RT具有显着的抗炎作用，可抑制白细胞募集，在0.3 Gy时最大。这种作用部分是由于TGF-β1产生增加，与ICAM-1表达的调节无关。

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