title: In vitro and in vivo protective effects of granulocyte colony-stimulating factor against radiation-induced intestinal injury.
abstract: Intestinal injury is a major cause of death after high-dose radiation exposure. The use of granulocyte-colony stimulating factor (G-CSF) to treat radiation injury has focused on enhancing recovery from hematopoietic radiation syndrome. We evaluated G-CSF for its ability to protect against radiation-induced intestinal injury in rat intestinal epithelial cells (IEC-6) and BALB/c mouse models. For in vitro tests, pre-radiation addition of G-CSF to IEC-6 prevented cytotoxicity and the loss of cell viability. Pre-radiation G-CSF treatment also reduced radiation-induced cleavage of caspase-3 and p53 in IEC-6. For in vivo tests, examination 12 h after abdominal irradiation showed that G-CSF-treated mice were protected against apoptosis of the jejunal crypts. G-CSF-treated mice also showed attenuated intestinal morphological changes 3.5 days after abdominal radiation (10 Gy). G-CSF also reduced the levels of proinflammatory cytokines interleukin-6 and tumor necrosis factor-α after radiation. This study showed that G-CSF may protect against radiation-induced intestinal damage through its anti-apoptotic and anti-inflammatory effects. These results suggest that G-CSF is promising candidate for protection against intestinal mucosal injury following irradiation.
authors.affiliation: Research Center, Dongnam Institute of Radiological & Medical Sciences (DIRAMS), Busan, 619-953, Republic of Korea, jskim@dirams.re.kr.
authors.forename: Joong-Sun
authors.initials: JS
authors.lastname: Kim
authors.forename: Miyoung
authors.initials: M
authors.lastname: Yang
authors.forename: Chang-Geun
authors.initials: CG
authors.lastname: Lee
authors.forename: Sung-Dae
authors.initials: SD
authors.lastname: Kim
authors.forename: Jung-Ki
authors.initials: JK
authors.lastname: Kim
authors.forename: Kwangmo
authors.initials: K
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism; D007583:Jejunum / Q000187:drug effects* / Q000293:injuries / Q000473:pathology; D008297:Male; D051379:Mice; D011833:Radiation Injuries, Experimental / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D011837:Radiation-Protective Agents; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D053148:Caspase 3