中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2010年
3期
239-242
,共4页
李明%欧红玲%邢爽%黄海潇%熊国林%谢玲%赵燕芳%赵振虎%王宁%王金香%缪竞诚%朱南康%罗庆良%从玉文%张学光
李明%歐紅玲%邢爽%黃海瀟%熊國林%謝玲%趙燕芳%趙振虎%王寧%王金香%繆競誠%硃南康%囉慶良%從玉文%張學光
리명%구홍령%형상%황해소%웅국림%사령%조연방%조진호%왕저%왕금향%무경성%주남강%라경량%종옥문%장학광
急性放射病%细胞因子%造血损伤%ED34+细胞%细胞周期%细胞凋亡%比格犬
急性放射病%細胞因子%造血損傷%ED34+細胞%細胞週期%細胞凋亡%比格犬
급성방사병%세포인자%조혈손상%ED34+세포%세포주기%세포조망%비격견
Acute radiation sickness%Cytokines%Hematopoietic injuries%CD34+cells%Cell cycle%Apoptosis%Beagles
目的 探讨多种细胞因子配伍应用治疗4.5 Gyγ射线照射比格犬造血系统损伤的作用及可能机制.方法 16只比格犬均给予4.5 Gy60Coγ射线全身照射,随机分为照射对照、综合对症和细胞因子3组.细胞因子组在综合对症支持治疗的基础上应用rhG-CSF、rhIL-11和rhIL-2联合治疗,采用流式细胞术检测外周血中CD34+细胞含量、有核细胞周期及凋亡比例.结果 4.5 Gyγ射线照射犬外周血中CD34+细胞含量在照射后1 d明显下降(照射对照组和综合对症组分别为照前值的61.3%和52.1%),G0/G1期有核细胞比例增加(分别为99.27%和99.49%),且凋亡率(分别为26.93%和21.29%)和坏死率(分别为3.27%和4.14%)明显升高(与照前值比较,P<0.05);而经过细胞因子治疗后,外周血中CD34+细胞含量在照射后1 d即明显升高(为照前值的135.6%),G0/G1期有核细胞比例(99.71%)进一步增加,其凋亡率(5.66%)和坏死率(1.60%)明显低于照射对照和综合对症组.结论 本研究的细胞因子组合可能通过动员骨髓中CD34+细胞到外周血,使细胞周期阻滞在G0/G1期,减少细胞凋亡,从而促进极重度骨髓型急性放射病犬造血功能的恢复.
目的 探討多種細胞因子配伍應用治療4.5 Gyγ射線照射比格犬造血繫統損傷的作用及可能機製.方法 16隻比格犬均給予4.5 Gy60Coγ射線全身照射,隨機分為照射對照、綜閤對癥和細胞因子3組.細胞因子組在綜閤對癥支持治療的基礎上應用rhG-CSF、rhIL-11和rhIL-2聯閤治療,採用流式細胞術檢測外週血中CD34+細胞含量、有覈細胞週期及凋亡比例.結果 4.5 Gyγ射線照射犬外週血中CD34+細胞含量在照射後1 d明顯下降(照射對照組和綜閤對癥組分彆為照前值的61.3%和52.1%),G0/G1期有覈細胞比例增加(分彆為99.27%和99.49%),且凋亡率(分彆為26.93%和21.29%)和壞死率(分彆為3.27%和4.14%)明顯升高(與照前值比較,P<0.05);而經過細胞因子治療後,外週血中CD34+細胞含量在照射後1 d即明顯升高(為照前值的135.6%),G0/G1期有覈細胞比例(99.71%)進一步增加,其凋亡率(5.66%)和壞死率(1.60%)明顯低于照射對照和綜閤對癥組.結論 本研究的細胞因子組閤可能通過動員骨髓中CD34+細胞到外週血,使細胞週期阻滯在G0/G1期,減少細胞凋亡,從而促進極重度骨髓型急性放射病犬造血功能的恢複.
목적 탐토다충세포인자배오응용치료4.5 Gyγ사선조사비격견조혈계통손상적작용급가능궤제.방법 16지비격견균급여4.5 Gy60Coγ사선전신조사,수궤분위조사대조、종합대증화세포인자3조.세포인자조재종합대증지지치료적기출상응용rhG-CSF、rhIL-11화rhIL-2연합치료,채용류식세포술검측외주혈중CD34+세포함량、유핵세포주기급조망비례.결과 4.5 Gyγ사선조사견외주혈중CD34+세포함량재조사후1 d명현하강(조사대조조화종합대증조분별위조전치적61.3%화52.1%),G0/G1기유핵세포비례증가(분별위99.27%화99.49%),차조망솔(분별위26.93%화21.29%)화배사솔(분별위3.27%화4.14%)명현승고(여조전치비교,P<0.05);이경과세포인자치료후,외주혈중CD34+세포함량재조사후1 d즉명현승고(위조전치적135.6%),G0/G1기유핵세포비례(99.71%)진일보증가,기조망솔(5.66%)화배사솔(1.60%)명현저우조사대조화종합대증조.결론 본연구적세포인자조합가능통과동원골수중CD34+세포도외주혈,사세포주기조체재G0/G1기,감소세포조망,종이촉진겁중도골수형급성방사병견조혈공능적회복.
Objective To investigate the mechanism of treatment of granulocyte colony-stimulating factor(rhG-CSF),recombinant human interleukin-11(rhIL-11)and recombinant human interleukin-2 (rhIL-2)on hematopoietic injuries induced by 4.5 Gy60 Coγ-ray irradiation in beagles,and to provide experimental evidence for the clinical treatment of extremely severe myeloid acute radiation sickness (ARS).Methods Sixteen beagle dogs were given 4.5 Gy60 Co γ-ray total body irradiation(TBI),then randomly assigned into irradiation control group,supportive care group or cytokines+supportive care (abbreviated as cytokines)group.In addition to supportive care,rhG-CSF,rhlL-11 and rhIL-2 were administered subcutaneously to treat dogs in cytokines group.The percentage of CD34+cells,cell cycle and apoptosis of nucleated cells in peripheral blood were examined by Flow cytometry.Results After 4.5 Gy 60 Co γ-ray irradiation,the CD34+cells in peripheral blood declined obviously(61.3%and 52.1% of baseline for irradiation control and supportive care group separately).The cell proportion of nucleated cells in Go/G1 phase was increased notably(99.27% and 99.49% respectively).The rate of apoptosis(26.93% and 21.29% separately)and necrosis(3.27% and 4.14%,respectively)of nucleated cells were elevated significantly when compared with values before irradiation(P<0.05) 1 d post irradiation.When beagles were treated with cytokines and supportive care,the CD34+cells in peripheral blood were markedly increased(135.6% of baseline).The effect of G0/G1 phase blockage of nucleated cells became more serious(99.71%).The rate of apoptosis(5.66%)and necrosis(1.60%)of nucleated cells were significantly lower than that of irradiation control and supportive care groups 1 d after exposure.Conclusions Cytokines maybe mobilize CD34+cells in bone marrow to peripheral blood,indce cell cycle block at G0/G1 phase and reduce apoptosis,and eventually cure hematopoieticinjuries induced by irradiation.
