Enhanced hematopoietic recovery in irradiated mice pretreated with interleukin-1 (IL-1)

Data in this report compare the number of colony-forming cells (CFC) in bone marrow from irradiated and pre-irradiated C57Bl/6J mice injected with saline or recombinant interleukin-1-alpha (rIL-1). Eight to 12 days after sublethal or lethal irradiation, there were more CFU-E (colony-forming units-erythroid), BFU-E (burst-forming units erythroid), GM-CFC (granulocyte-macrophage colony-forming cells), and day 8 CFU-S (colony-forming units-spleen) in bone marrow from rIL-1 injected mice than from saline injected mice. Prior to irradiation, there was no increase in number of CFC in bone marrow from rIL-1 injected mice. However, as determined by sensitivity to hydroxyurea, rIL-1 injection stimulated GM-CFC into cell cycle. These results demonstrate that rIL-1 injection increases the number of CFC that survive in irradiated mice and may be a consequence of the stimulation of CFC into cell cycle prior to irradiation.     

Enhanced Hematopoietic Recovery in Irradiated Mice Pretreated with Interleukin-1 (IL-1)

Data in this report compare the number of colony-forming cells (CFC) in bone marrow from irradiated and pre-irradiated C57B1/6J mice injected with saline or recombinant interleukin-1-alpha (rlL-1). Eight to 12 days after sublethal or lethal irradiation, there were more CFU-E (colony-forming units-erythroid), BFU-E (burst-forming units erythroid), GM-CFC (granulocyte-macrophage colony-forming cells), and day 8 CFU-S (colony-forming units-spleen) in bone marrow from rIL-1 injected mice than from saline injected mice. Prior to irradiation, there was no increase in number of CFC in bone marrow from rIL-1 injected mice. However, as determined by sensitivity to hydroxyurea, rIL-1 injection stimulated GM-CFC into cell cycle. These results demonstrate that rIL-1 injection increases the number of CFC that survive in irradiated mice and may be a consequence of the stimulation of CFC into cell cycle prior to irradiation.     

Enhanced Hematopoietic Recovery in Irradiated Mice Pretreated with Interleukin-1 (IL-1)

Abstract

Data in this report compare the number of colony-forming cells (CFC) in bone marrow from irradiated and pre-irradiated C57B1/6J mice injected with saline or recombinant interleukin-1-alpha (rlL-1). Eight to 12 days after sublethal or lethal irradiation, there were more CFU-E (colony-forming units-erythroid), BFU-E (burst-forming units erythroid), GM-CFC (granulocyte-macrophage colony-forming cells), and day 8 CFU-S (colony-forming units-spleen) in bone marrow from rIL-1 injected mice than from saline injected mice. Prior to irradiation, there was no increase in number of CFC in bone marrow from rIL-1 injected mice. However, as determined by sensitivity to hydroxyurea, rIL-1 injection stimulated GM-CFC into cell cycle. These results demonstrate that rIL-1 injection increases the number of CFC that survive in irradiated mice and may be a consequence of the stimulation of CFC into cell cycle prior to irradiation.     

流式细胞术测定PF4对放射损伤小鼠骨髓造血细胞的保护作用

目的研究血小板第4因子(PF4)对     

~(60)Co-γ射线照射对小鼠SVZ神经干细胞增殖的影响

目的:探讨60Co-γ射线照射对成体小鼠侧脑室室管膜下区(SVZ)神经干细胞增殖的影响。方法:28只昆明小鼠随机分成4组,每组7只,分别以0 Gy、5 Gy(小剂量)、15 Gy(中剂量)、30 Gy(大剂量)剂量进行照射,于照射后1周观察侧脑室室管膜下区(SVZ)的5-溴脱氧核苷尿嘧啶(BrdU)阳性细胞形态和数目。结果:照射后1周,各照射组SVZ的BrdU阳性细胞形态与对照组无差别,呈圆形、椭圆形以及梭形等;15 Gy、30 Gy照射组SVZ的BrdU阳性细胞数明显降低(P<0.01),5 Gy照射组SVZ的BrdU阳性细胞数无差别(P>0.05)。结论:大中剂量60Co-γ照射会抑制SVZ神经干细胞的增殖分裂能力。     

Androstenediol stimulates myelopoiesis and enhances resistance to infection in gamma-irradiated mice

The ionizing radiation-induced hemopoietic syndrome is characterized by defects in immune function and increased mortality due to infections and hemorrhage. Since the steroid 5-androstene-3beta, 17beta-diol (5-androstenediol, AED) modulates cytokine expression and increases resistance to bacterial and viral infections in rodents, we tested its ability to promote survival after whole-body ionizing radiation in mice. In unirradiated female B6D2F1 mice, sc AED elevated numbers of circulating neutrophils and platelets and induced proliferation of neutrophil progenitors in bone marrow. In mice exposed to whole-body (60)Co gamma-radiation (3 Gy), AED injected 1 h later ameliorated radiation-induced decreases in circulating neutrophils and platelets and marrow granulocyte-macrophage colony-forming cells, but had no effect on total numbers of circulating lymphocytes or erythrocytes. In mice irradiated (0, 1 or 3 Gy) and inoculated four days later with Klebsiella pneumoniae, AED injected 2 h after irradiation enhanced 30-d survival. Injecting AED 24 h before irradiation or 2 h after irradiation increased survival to approximately the same extent. In K. pneumoniae-inoculated mice (irradiated at 3-7 Gy) and uninoculated mice (irradiated at 8-12 Gy), AED (160 mg/kg) injected 24 h before irradiation significantly promoted survival with dose reduction factors (DRFs) of 1.18 and 1.26, respectively. 5-Androstene-3beta-ol-17-one (dehydroepiandrosterone, DHEA) was markedly less efficacious than AED in augmenting survival, indicating specificity. These results demonstrate for the first time that a DHEA-related steroid stimulates myelopoiesis, and ameliorates neutropenia and thrombocytopenia and enhances resistance to infection after exposure of animals to ionizing radiation.     

Stimulated hemopoiesis and enhanced survival following glucan treatment in sublethally and lethally irradiated mice

Hemopoietic effects of the reticuloendothelial agent glucan were assayed in normal mice and in mice hemopoietically depleted by exposure to 60Co radiation. In normal mice, glucan administration increased the content of bone marrow and splenic transplantable pluripotent hemopoietic stem cells (CFU-s), committed granulocyte-macrophage progenitor cells (GM-CFC), and pure macrophage progenitor cells (M-CFC). Erythroid progenitor cells (CFU-e) were increased only in the spleen. In sublethally irradiated mice (650 rads), glucan increased the number of endogenous pluripotent hemopoietic stem cells (E-CFU) when administered either before or after irradiation. The most pronounced effects were observed when glucan was administered 1 day before, 1 h before, or 1 h after irradiation. In addition, the administration of glucan before lethal irradiation (900 rads) enhanced survival. The most significant results were seen when glucan was administered 1 day prior to irradiation. The possibility of using agents such as glucan to enhance hemopoietic reconstitution and prevent septicemia following chemotherapy and/or radiotherapy is discussed.     

脉冲式低剂量率照射对食管癌细胞及肺组织的影响

目的:评估脉冲式低剂量率照射（RLDR）对食管癌细胞及小鼠正常肺组织的影响。方法:针对人食管癌细胞系EC109和SPF级KM小鼠,进行4种模式照射:常规（CR, 5×2 Gy）、大分割（HR, 2×5 Gy）、PLDR［5×（10×0.2） Gy,当日每分次间隔3 min］、对照组（CG, 0 Gy）。分别于照射前、10 Gy照射后第1、3、5、7天使用CCK-8法检测EC109细胞增殖水平,第4周使用ELISA法检测小鼠血清转化生长因子β1（TGF-β1）水平以及H&E染色观察其肺组织形态。结果:EC109照射后第3天起各实验组的相对吸光度、细胞活力显著低于CG（P<0.05）;照射后第5、7天的CR与PLDR的相对吸光度、细胞活力均显著高于HR组（P<0.05）;CR与PLDR之间均无明显差异（P>0.05）。照射结束后第4周CR、HR小鼠肺组织出现肺泡壁增厚、较多炎细胞浸润,PLDR组小鼠肺组织较正常;且CR与HR小鼠血清TGF-β1水平明显高于CG与PLDR（P<0.05）,PLDR与CG无统计学差异（P>0.05）。结论:与CR、HR相比,PLDR在有效抑制食管癌细胞增殖的同时可显著降低放射性肺损伤。     

骨髓间质干细胞输注对外周血干细胞移植造血恢复的影响

目的:观察骨髓间质干细胞 (MSCs)输注对外周血干细胞移植 (PBSCT)后造血恢复的影响。方法:去脾小鼠经粒细胞集落刺激因子动员后收获外周血单个核细胞 (PBMC)和扩增培养的骨髓间质干细胞 (MSCs),移植给经放 /化疗预处理的BALB/c小鼠,数量分别为10⁶PBMC(PBSCT组)、10⁴MSCs和10⁶ PBMC(实验1组)、10⁶ MSCs和10⁶ PBMC(实验 2组),观察受体鼠 4周的生存率、骨髓有核细胞 (BMNC)、粒细胞巨噬细胞集落形成单位 (CFU-GM)、成纤维细胞集落形成单位 (CFU-F)、外周血白细胞 (WBC)计数等指标。结果:实验 2组的生存率、BMNC、CFU-GM、CFU-F显著高于PBSCT组,WBC计数恢复较PBSCT组快 (P <0.05);实验1组和PBSCT组比较,WBC计算恢复快,CFU-F产率高 (P <0.05)。结论:骨髓间质干细胞输注有促进外周血干细胞移植造血恢复的作用。     

X线对仔鼠胃组织结构及总抗氧化能力、谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性的影响

目的 观察X线辐射后仔鼠胃组织结构和总抗氧化能力(T-AOC)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽还原酶(GR)的动态变化,为电离辐射防护提供实验依据.方法 对160只仔鼠(出生6～7d)用不同吸收剂量(0Gy、1Gy、3Gy、5Gy、7Gy) X线进行全身辐射,分别于辐射后1d、5d、10d和20d,用比色法检测仔鼠胃组织中T-AOC、GSH-PX、GR酶活性的变化,用显微技术观察仔鼠胃组织结构的变化.结果 1Gy辐射组仔鼠胃T-AOC活性在1～20d时高于对照组,差异显著(P＜0.05),GR活性在1～10d时高于对照组,差异显著(P＜0.05),其他各辐射组T-AOC和GR在辐射后始终低于对照组,差异显著或极显著(P＜0.05或P＜0.01);1Gy辐射组仔鼠胃GSH-PX活性在辐射后1d时低于对照组,差异显著(P＜0.05),以后高于对照组,差异显著(P＜0.05);3Gy辐射组GSH-PX在辐射后1d时高于对照组,差异显著(P＜0.05),以后始终低于对照组,差异显著或极显著(P＜0.05或P＜0.01);其他各辐射组GSH-PX活性始终低于对照组,差异极显著(P＜0.01).随着辐射剂量的增大,实验组仔鼠胃黏膜上皮和腺体均有不同程度的变化,上皮肿胀、空泡化、脱落,胃底腺细胞排列松散、部分降解,胃出血.结论 X线辐射影响仔鼠胃组织结构,这可能与胃抗氧化酶活性降低有关.     

Pathological evaluation of WR-151327 administered orally in irradiated and non-irradiated male mice.

Studies were made on the radioprotective and toxic effects of orally administered WR-151327 in male CD2F1 mice. The lowest dose of orally administered drug permitting probit analysis of data was 450 mg per kg. The calculated radioprotective dose reduction factors (DRF) at 450 mg per kg and 900 mg per kg of body weight (BW) WR-151327 were 1.2 and 1.3, respectfully. Pathological examination at 8, 30 or 90 days post administration of 100, 450, or 900 mg per kg of the drug demonstrated that the major target organ for orally dosed mice was the testes. There was a decrease in the number of cells in the germinal cell layers of testes from animals administered 450 mg per kg WR-151327 or 10 Gy whole body irradiation after eight days. Moreover, there was a dramatic reduction in the germinal cells in mice seminiferous tubules treated with a combination of 450 mg per kg WR-151327 plus 10 Gy radiation after eight days.     

X线电离辐射通过上调c-Myc表达促进肺癌A549细胞上皮间质转化

目的:探讨电离辐射对肺癌A549细胞上皮间质转化(EMT)的影响及其可能机制。方法:采用不同剂量(0 Gy、1 Gy、2 Gy、4 Gy和8 Gy)的X射线分别照射肺癌A549细胞不同时间,通过倒置显微镜观察X射线照射12 h、24 h和48 h时肺癌A549细胞形态的改变;Western blot检测X射线照射12 h与24 h时EMT相关蛋白vimentin、N-cadherin及E-cadherin和转录因子c-Myc的表达。结果:照射后肺癌A549细胞轮廓不清,突起增多,边缘不规则且呈煎蛋样塌陷,以8 Gy X射线照射48 h时肺癌A549细胞上皮间质化形态最明显。与0 Gy照射剂量对照组相比,vimentin虽然于4 Gy剂量照射12 h时下调,但是处理24 h时各剂量照射组vimentin均表现为上调,其中2 Gy剂量照射组其上调最明显(P0.01);与0 Gy照射剂量对照组相比,1 Gy、2 Gy及4 Gy照射组照射肺癌A549细胞24 h后其N-cadherin表达上调(P0.05);各照射剂量对肺癌A549细胞E-cadherin表达没有显著影响。照射24 h后肺癌A549细胞c-Myc表达上调,以4 Gy剂量照射组表达差异最明显(P0.01)。结论:X线电离辐射可能通过上调c-Myc表达促进肺癌A549细胞发生上皮间质转化。     

Radioprotection by oral administration of Aegle marmelos (L.) Correa in vivo.

The radioprotective effect of an extract of Aegle marmelos (L.) Correa (AME), family Rutaceae, was investigated in mice exposed to different doses of gamma-radiation. Mice were administered orally AME 250 mg/kg b.wt. orally daily for 5 consecutive days before exposure to 6, 7, 8, 9, 10, or 11 Gy of gamma-radiation. The animals were monitored daily up to 30 days after irradiation for the development of symptoms of radiation sickness or death. Treatment of mice with AME before irradiation reduced the symptoms of radiation sickness and delayed death compared to the irradiated controls given sterile physiological saline (SPS). AME provided protection against both gastrointestinal and hematopoietic toxicities. Reducing the administration schedule of AME to 1 or 3 consecutive days or increasing the schedule to 7 consecutive days was not as effective as 5 consecutive days of preradiation schedule. The administration of AME after irradiation was not effective, and no survivors could be reported 30 days after irradiation. The LD50/30 was found to be 8.1 Gy for the SPS + irradiation group and 9.7 Gy for the AME + irradiation group. The oral administration of AME resulted in an increase in radiation tolerance by 1.6 Gy, and the dose reduction factor was found to be 1.2. Preradiation treatment of mice with AME caused a significant depletion in lipid peroxidation followed by a significant elevation in glutathione concentration in the liver of mice 31 days after irradiation. The drug was nontoxic up to a dose of 6000 mg/kg b.wt., the highest drug dose that could be tested for acute toxicity.     

非黏附骨髓源干细胞治疗急性放射损伤

背景：目前对于辐射剂量超过8 Gy的急性放射病尚缺乏有效的治疗方案,间充质干细胞可以分泌多种造血因子、重建造血,在放射损伤救治中具有重要意义。 目的：探讨非黏附骨髓源干细胞在8.5 Gy X射线照射所致急性骨髓型放射损伤救治中的作用及作用机制。 方法：取胎儿四肢长骨的非黏附骨髓源干细胞,分析其麦面抗原,细胞周期,成骨和成脂分化潜能,以及血管内皮生长因子及Annexin A2表达。BALB/C小鼠受8.5 Gy一次性全身均匀X射线照射后随机分成骨髓源干细胞组和对照组,骨髓源干细胞组小鼠在X射线照射2 h内经尾静脉输注含3×106 CFDA-SE标记的人非黏附骨髓源干细胞的细胞悬液0.3 mL,对照组小鼠在X射线照射2 h内输注0.3 mL生理盐水。观察骨髓源干细胞的分布情况、小鼠的存活率、白细胞变化、骨髓病理变化及骨髓中新生血管形成情况。 结果与结论：X射线照射后移植的非黏附间充质干细胞可以向损伤部位归巢;骨髓源干细胞组小鼠存活率明显高于对照组;与对照组相比,骨髓源干细胞组小鼠外周血白细胞计数下降慢且恢复迅速,X射线照射后14 d左右达最低,30 d基本恢复至正常水平。X射线照射后21 d,骨髓源干细胞组骨髓增生活跃,骨髓腔内新生造血灶显著多于对照,血管密度亦显著高于对照组。说明人胎儿非黏附骨髓源干细胞促进急性放射损伤小鼠骨髓内新生血管形成,改善并加快受损小鼠造血功能的恢复。     

重组人血管内皮抑素联合放疗对Lewis肺癌小鼠肿瘤生长及VEGF表达的影响

目的:研究重组人血管内皮抑素(rh-Endostatin,YH-16,恩度)对不同放射剂量治疗的Lewis肺癌小鼠肿瘤生长及血管内皮生长因子(VEGF)表达的影响。方法:制作Lewis肺癌细胞接种肿瘤的动物模型,并将60只模型小鼠随机分为5组:A,空白对照组(不予任何治疗);B,小剂量多次放疗组(1Gy/f,隔日一次,共4次);C,大剂量单次放疗组(4Gy/f,共1次);D,小剂量多次放疗联合恩度组(放疗前4天起每天右侧腹股沟区皮下注射恩度0.1ml,共15天,放射剂量为1Gy/f,隔日一次,共4次);E,大剂量单次放疗联合恩度组(放疗前4天起每天右侧腹股沟区皮下注射恩度0.1ml,共15天,放射剂量为4Gy/f,共1次)。分别给予上述处理后计算抑瘤率,并用免疫组化SP法测定各组VEGF的阳性表达率。结果:与C、E组比较,B、D组的抑瘤作用及VEGF表达下降明显(P<0.05),尤以D组抑瘤更强(P<0.05)、VEGF下降最多(P<0.05)。结论:放疗前使用恩度可使Lewis肺癌小鼠对放疗的敏感性增加,其机制可能与下调VEGF的表达有关。     

川芎嗪对急性放射损伤小鼠骨髓中LFA- 1、ICAM-1表达影响的研究

目的：探讨川芎嗪对急性放射损伤小鼠骨髓中LFA-1、 ICAM-1表达水平的影响及其促进骨髓造血重建的机制。方法:正常24只清洁级昆明小鼠随机分为3组：正常组、生理盐水组和川芎嗪组。正常组未作任何处理，将生理盐水组和川芎嗪组小鼠用6.0 Gy ［⁶⁰Co］γ射线1次性全身均匀照射，吸收剂量率为0.56 Gy/min。照射后即分别喂饲相同剂量的生理盐水（0.2 mL/只，每天2次）和川芎嗪（2 mg/只，每天2次），直至处死为止。在照射后第7、14、21 d处死小鼠，制备骨髓细胞悬液，培养基质细胞，用RT-PCR、Western blotting方法检测骨髓基质细胞ICAM-1mRNA及其蛋白表达水平，用流式细胞仪检测骨髓单个核细胞表面LFA-1表达水平。结果:6.0 Gy ［⁶⁰Co］ γ 射线照射后，川芎嗪组骨髓单个核细胞表面 LFA-1表达水平均显著高于生理盐水组(P<0.01或P<0.05) ；骨髓基质细胞ICAM-1mRNA及其蛋白表达水平均明显低于生理盐水组（P<0.01或P<0.05）。结论:川芎嗪加快辐射后骨髓单个核细胞表面LFA-1的表达，降低骨髓基质细胞ICAM-1的表达，从而改善骨髓微环境，促进造血重建。     

Effects of radiation and latent virus on immune responses in a space flight model

BACKGROUND: The immunosuppressive effects of space flight radiation and reactivation of latent virus infections in human beings are largely unknown. OBJECTIVE: To develop a murine model that can predict the adverse effects of space flight radiation and reactivation of latent virus infection for human beings. METHODS: In experiment I, some BALB/c mice received whole-body gamma-irradiation (3 Gy) on day 0 and murine polyoma virus (PyV) on day 1. In experiment II, mice received irradiation (3 Gy) or none on days 0 and/or 49, and PyV or none on day 1: A1, 3 Gy/PyV/3 Gy; A2, 3 Gy/ PyV/0 Gy; B1, 0 Gy/PyV/3 Gy; B2, 0 Gy/ PyV/0 Gy; C, 3 Gy/0 PyV/0 Gy; and D, 0 Gy/0 PyV/0 Gy. RESULTS: In experiment I, PyV was detected by PCR more frequently in several host organs tested and for a longer period of time in irradiated than in control animals. In experiment II, PyV replication in the spleen was detected in A1>B1 mice on days 10 and 20; both groups cleared PyV by day 49. After irradiation on day 49, reactivated PyV was detected in more B1 than A1 mice. A1 mice had lower spleen weights and cell counts than other groups at all time points. From 0 to 49 days, irradiation suppressed spleen cell proliferation to concanavalin A in all irradiated groups except in B1 when the virus was cleared at day 20. PyV enhanced IFN-gamma production in all groups: B1>A1>C, D (0-49 days; all differences, P < .05). CONCLUSION: This small animal model of space flight suggests that the combined effects of radiation and virus replication will significantly affect T-lymphocyte-mediated immunity that may lead to chronic viral infection and malignancy.     

Regeneration of hyaline articular cartilage with irradiated transforming growth factor beta1-producing fibroblasts

The regeneration of hyaline articular cartilage by cell-mediated gene therapy using transforming growth factor beta(1) (TGF-beta(1))-producing fibroblasts (NIH 3T3-TGF-beta(1)) has been reported previously. In this study, we investigated whether TGF-beta(1)-producing fibroblasts irradiated with a lethal dose of radiation are still capable of inducing the regeneration of hyaline articular cartilage. NIH 3T3TGF-beta(1) fibroblasts were exposed to doses of 20, 40, or 80 Gy, using a irradiator, and then injected into artificially made partial defects on the femoral condyle of rabbit knee joints. The rabbits were killed 3 or 6 weeks postinjection and hyaline articular cartilage regeneration was evaluated by histological and immunohistochemical staining (n = 5 per each group). Irradiated NIH 3T3-TGFbeta(1) fibroblasts started to die rapidly 3 days after irradiation; moreover, the kinetics of their viability were similar regardless of the radiation intensity. TGF-beta1 expression, measured by ELISA, showed that the TGF-beta(1) protein produced from the irradiated cells peaked 5 days after irradiation and thereafter declined rapidly. Complete filling of the defect with reparative tissue occurred in all the groups, although variations were observed in terms of the nature of the repair tissue. Histological and immunohistochemical staining of the repair tissue showed that the tissue newly formed by irradiated NIH 3T3-TGF-beta(1) fibroblasts after exposure to 20 Gy had hyaline cartilage-like characteristics, as was observed in the nonirradiated controls. On the other hand, the repair tissue formed by NIH 3T3-TGF-beta(1) fibroblasts irradiated with 40 or 80 Gy showed more fibrous cartilage-like tissue. These results suggest that TGF-beta(1)-producing fibroblasts irradiated up to a certain level of lethal dose (i.e., 20 Gy) are able to induce normal-appearing articular cartilage in vivo. Therefore, irradiated heterologous cell-mediated TGF-beta(1) gene therapy may be clinically useful and an efficient method of regenerating hyaline articular cartilage.     

Evaluation of insulin-like growth factor-1 for prevention of radiation-induced spinal cord damage

AIM: To test whether insulin-like growth factor-1 (IGF-1) ameliorates radiation-induced spinal cord myelopathy and to establish the dose-effect relationship for this growth factor which has not been administered in conjunction with spinal cord irradiation to date. METHODS: Animal experiments were conducted to test the feasibility of IGF-1 injection in a model of cervical spinal cord irradiation in adult Fisher F-344 rats and to determine the most effective dose level of IGF-1. Irradiation was given in two fractions (16 Gy followed by 18 Gy) and animals were examined for the development of paresis (follow-up 12 months). RESULTS: The dose-finding experiment revealed significant differences in the incidence of radiation myelopathy (RM). The most effective dose of IGF-1 was 50 microg per day. CONCLUSIONS: IGF-1 showed promising activity as a radioprotective agent in a model of high-dose spinal cord irradiation. Further studies are needed to examine the results with multiple small doses of radiation as widely applied in clinical protocols.     

EL9611红白血病小鼠急性GVHD动物模型的建立

目的: 建立EL9611红白血病小鼠急性移植物抗宿主病(GVHD)的动物模型。方法: 同种异基因骨髓移植(allo-BMT)以C57BL/6(H-2^b)鼠为供鼠,BALB/c(H-2^d)为受鼠。设白血病组(n=10)、照射对照组(白血病鼠照射后不进行allo-BMT,n=4)、GVHD组(白血病鼠照射+allo-BMT,n=10)及正常对照组(n=4)。白血病组采用每只BALB/c鼠尾静脉输注2×10⁶个EL9611红白血病细胞建立红白血病动物模型;GVHD组于接种白血病细胞7 d后行总剂量为8.0 Gy的1次性 γ射线全身照射(TBI),照射后5 h内每只小鼠尾静脉输注C57BL/6鼠骨髓细胞2×10⁶个＋脾细胞1×10⁷个,建立EL9611红白血病小鼠的急性GVHD动物模型。观察小鼠体位、皮毛、大便等临床表现,病理检查肝脾、皮肤、小肠、外周血和骨髓,计算生存率。结果: 白血病组生存时间(14.5±2.1) d ,生存时间与GVHD组相比P<0.01,死亡率100％,无自发缓解,死亡时肝脾肿大(肝重2.40 g±0.48 g,脾重0.84 g±0.20 g,与正常对照组比P<0.01),外周血WBC升高 ,病理检查示组织正常结构破坏,白血病细胞浸润。照射对照组生存时间为(9.0±0.7) d,生存时间与GVHD组和正常对照组相比差异显著(P<0.01),死亡率100％,病理检查显示造血衰竭。GVHD组生存时间为(32.0±3.2)d,生存时间与其它各组相比P<0.01,死亡率100％,allo-BMT后第10-13 d出现症状,临床表现和病理检查符合Ⅰ到Ⅱ度GVHD的改变。结论: 采用EL9611红白血病细胞(2×10⁶/鼠)静脉输注的方式可成功建立EL9611红白血病动物模型;接种EL9611红白血病细胞第7 d行TBI +allo-BMT可成功建立EL9611红白血病小鼠的急性GVHD动物模型。