Research Center, Dongnam Institute of Radiological & Medical Sciences (DIRAMS), Busan 619-953, Republic of Korea.
Food Chem Toxicol. 2012 Sep;50(9):3174-80. doi: 10.1016/j.fct.2012.05.059. Epub 2012 Jun 12.
Gastrointestinal injury is a major cause of death following exposure to high levels of radiation, and no effective treatments are currently available. In this study, we examined the capacity of granulocyte colony-stimulating factor (G-CSF) to mitigate intestinal injury in, and improve survival of, C3H/HeN mice given a lethal dose (12 Gy) of radiation to the abdomen. G-CSF (100 μg/kg body weight) was injected subcutaneously daily for 3 days after irradiation and shown to improve survival and intestinal morphology at 3.5 days compared with saline-injected controls. The morphological features improved by G-CSF included crypt number and depth, villous length, and the length of basal lamina of 10 enterocytes. G-CSF also normalized the levels of circulating tumor necrosis factor alpha and attenuated the loss of peripheral neutrophils, caused by radiation-induced myelosuppression. In conclusion, our results suggest that G-CSF enhanced the survival of irradiated mice and minimized the effects of radiation on gastrointestinal injury.
胃肠道损伤是暴露于高水平辐射后死亡的主要原因,目前尚无有效的治疗方法。在这项研究中,我们研究了粒细胞集落刺激因子 (G-CSF) 减轻腹部接受致死剂量 (12 Gy) 辐射的 C3H/HeN 小鼠肠道损伤和提高其存活率的能力。照射后每天皮下注射 G-CSF(100 μg/kg 体重)3 天,与生理盐水注射对照组相比,在 3.5 天时可提高存活率和肠道形态。G-CSF 改善的形态特征包括隐窝数量和深度、绒毛长度以及 10 个肠上皮细胞的基底膜长度。G-CSF 还可使循环肿瘤坏死因子-α的水平正常化,并减轻辐射诱导的骨髓抑制引起的外周中性粒细胞的损失。总之,我们的结果表明,G-CSF 增强了受照射小鼠的存活率,并最大限度地减少了辐射对胃肠道损伤的影响。