摘要
目的 研究rhIL 11对急性辐射损伤后骨髓造血细胞凋亡的影响。方法 应用原位末端标记、流式细胞术及琼脂糖凝胶电泳法分别在照射后不同时间观察了rhIL 11对 5 5Gy6 0 Coγ射线全身照射小鼠骨髓造血细胞凋亡的影响。应用免疫组织化学法观察了各组小鼠骨髓细胞Bcl 2和P5 3蛋白的表达变化。结果 ①照射前应用rhIL 11可使照射后 6h小鼠骨髓造血细胞凋亡率下降 ,而照射后给药组照射后 12h凋亡率下降更加明显。②照射后 3d给药组P5 3蛋白表达均较照射对照组明显降低 (P <0 0 1) ,Bcl 2蛋白表达则明显升高 ;照射后 7d给药组Bcl 2升高仍明显。结论应用rhIL 11可有效抑制照射后小鼠骨髓造血细胞凋亡 ,有利于造血功能的恢复。rhIL 11对细胞凋亡的影响可能与Bcl 2和P5 3等蛋白的调节密切相关。
Objective To evaluate the effect of rhIL-11 on apoptosis of bone marrow cells of mice irradiated with 5 ^5 Gy 60 Co γ rays. Methods At 6,12,24 hours and on days 3,7 after irradiation,apoptosis of bone marrow cells was studied by means of in situ terminal labeling,flow cytometry and DNA electrophoresis.The expressions of P53 and Bcl-2 of bone marrow cells were evaluated by immunocytochemistry. Results (1)There was a significant descending trend of apoptotic ratio in rhIL-11-treated group 6 and 12 hours after TBI compared with the control group.(2)On day 3,P53 was expressed at a significantly lowere level ( P< 0.01),whereas Bcl-2 at a significantly higher level ( P< 0.01),in rhIL-11-treated groups than those of the placebo controls,respectively.On day 7,expression of Bcl-2 was still higher in rhIL-11-administered-before-TBI group ( P< 0.01). Conclusion rhIL-11 can promote recovery of murine BM cells by protecting them from apoptosis.The effects of rhIL-11 on apoptosis may have close relationship to the modulation of Bcl-2 and P53. ;
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2004年第1期18-20,共3页
Chinese Journal of Radiological Medicine and Protection
基金
全军"十五"指令性基金资助项目 (0 1L0 19)