致死剂量的γ线照射后小鼠胸腺淋巴细胞的凋亡规律及与bax、bcl-2和Bcl-XL表达的关系

目的：观察致死剂量γ线照射后小鼠胸腺淋巴细胞凋亡特征及与Bax、Bcl-2和Bcl-XL蛋白和mRNA表达的关系，为急性重度以上放射病的治疗提供依据。方法：清洁级C57小鼠250只，随机分为0、6、9、12、15和20 Gy6个剂量组.经γ线全身1次照射后，于照射后1～28d和3～12个月，活杀取胸腺和外周血，用原位末端标记(TUNEL)和麦格-姬姆萨(MGG)染色检测胸腺淋巴细胞的凋亡：用原位杂交和碱性磷酸酶免疫组化染色法，检测Bax、Bcl-2和Bcl-XL mRNA和其蛋白的表达。结果.(1)各剂量组小鼠外周血白细胞在照射后6h，出现一过性的升高，以后迅速下降.6Gy照射后7d降至最低，至照射后28d基本恢复到正常水平：(2)不同剂量的γ线照射后24h，胸腺淋巴细胞的凋亡率迅速升高；在6～12Gy范围内与照射的剂量呈正比，≥15Gy照射后变化不明显。(3)6Gy照射后24h，胸腺淋巴细胞的凋亡率达高峰，而后开始降低；但直至照射后6个月和12个月，凋亡率仍明显高于对照组。(4)6Gy照射后3h，胸腺淋巴细胞中Bax蛋白的表达即出现增加，至24h达峰值，显示出时效关系；而Bcl-2蛋白于照射后3h即明显下降，24h降至最低；Bcl-XL蛋白也在照射后24h降至最低。bax和bel-2 mRNA的检测与蛋白水平的检测一致。结论：经6～12 Gy照射后，淋巴细胞的凋亡与照射剂量成正比，≥15 Gy照射后凋亡率下降，提示≤12 Gy照射后胸腺淋巴细胞的凋亡是其死亡的主要方式。促凋亡蛋白Bax表达的增加及抗凋亡蛋白Bcl-XL表达的下降，与照射剂量和淋巴细胞的凋亡率呈现较好的对应关系，提示它们在致死剂量的照射所致胸腺淋巴细胞凋亡的调控中起着重要作用。     

X射线全身照射对小鼠免疫功能的影响

目的:通过X-射线体外全身照射BALB/c小鼠建立小鼠辐射损伤模型,检测放射线对小鼠脾组织、单核巨噬细胞及T、B淋巴细胞损伤的剂量范围,探索放射线剂量与组织损伤程度之间的量效关系。方法:采用9种不同剂量的X-射线体外全身照射BALB/c小鼠,于照射后1d、60d、120d取腹腔细胞做大吞噬实验;分离脾细胞,MTT法检测T细胞增殖活性,同时取脾脏组织切片、HE染色,检测组织损伤程度;照射后120d取小鼠脾细胞用流式细胞仪检测T、B细胞数量百分比。结果:不同剂量X-射线照射的小鼠其大吞噬细胞的吞噬指数及T细胞的增殖指数之间均存在差异,且与放射剂量呈负相关性。FCM检测结果显示0.1Gy及以上剂量组与正常对照组相比较,小鼠T、B淋巴细胞数量减少(P<0.05)。0.25Gy和0.5Gy组T、B淋巴细胞数量明显高于除0.05Gy以外的其余各照射组,但是仍低于正常组(P<0.05)。脾组织切片显示,照射后1d 0.1Gy以上照射组脾脏炎性细胞浸润;60d后,4.0Gy和8.0Gy组脾脏明显萎缩、巨噬细胞增生、瘤样变,其余组损伤不明显;120d后8.0Gy组脾脏萎缩、红白髓分界不清,白髓损伤尤为严重,其余组不明显。结论:0.1Gy以上X-射线体外全身照射可引起小鼠免疫功能及组织损伤,且损伤程度与放射性强度呈剂量依赖性。     

丝裂霉素C对辐射损伤小鼠胸腺细胞的影响

目的：在选择辐射损伤小鼠胸腺细胞适宜剂量的基础上，观察丝裂霉素C（MMC）对辐射损伤小鼠胸腺细胞自发掺入的影响。 方法： 流式细胞仪检测小鼠胸腺细胞周期，选择辐射剂量；用［³H］-TdR掺入法研究MMC对辐射损伤小鼠胸腺细胞的作用。 结果： 选择用γ-射线1.5 Gy全身照射小鼠，建立辐射损伤模型。 0.04 μg/kg MMC对辐射损伤有拮抗作用，表现为0.04 μg/kg MMC+1.5 Gy照射组胸腺细胞自发掺入率明显高于生理盐水+1.5 Gy照射组。 结论： 一定剂量MMC可拮抗辐射损伤小鼠胸腺细胞。     

卷柏水部位对小鼠胸腺和脾脏的辐射防护作用

目的 观察卷柏水部位对受照射小鼠胸腺、脾脏细胞周期及凋亡率的影响.方法 设正常组、模型组、雌激素组和卷柏组;除正常组外,其它各组小鼠均接受6.0 Gy60Coy射线全身照射一次;各组小鼠分别于照射前72、48、24 h和照射后即刻灌服药物或蒸馏水.分别于照射后6、12、24 h立即断头处死小鼠,观察卷柏水部位对受照射小鼠胸腺、脾脏细胞周期及凋亡率的影响.结果 卷柏水部位可降低受照射小鼠胸腺、脾脏的Go/G1期细胞百分率,升高其G2/M、S期细胞百分率,也可明显降低其细胞凋亡率.结论 卷柏水部位可通过抑制细胞凋亡,调节受照射小鼠胸腺、脾脏的细胞周期进程,发挥其辐射防护作用.     

60Co放射及微量元素锌对钛种植体骨融合的影响

背景：前期实验证实补锌可以加速种植体的骨融合。目的：观察⁶⁰Co放射及微量元素锌对种植体骨融合的影响。方法：取成年雄性家兔36只,双侧胫骨近心端各植入1枚钛种植体,建立钛种植体动物模型,随机均分为4组,补锌组种植后24 h肌注10 g/L硫酸锌4 mg/kg,1次/d;对照组种植后24 h肌注9 g/L生理盐水4 mg/kg,1次/d;放射组于种植后第2,4,6天给予双侧胫骨近心段⁶⁰Co照射,15 Gy/d,同时种植后24 h肌注9 g/L生理盐水4 mg/kg,1次/d;放射补锌组于种植后第2,4,6天给予双侧胫骨近心段⁶⁰Co照射,15 Gy/d,同时种植后24 h肌注10 g/L硫酸锌4 mg/kg,1次/d。种植后1,4,12周利用显微镜观察种植体骨界面组织形态。结果与结论：在相同时间段内,与其他各组相比,放射组种植体周围成纤维细胞数量较多,纤维性结合较多,而骨性组织特别是成熟骨组织形成较少。在相同时间段内,与其他各组相比,补锌组种植体表面成骨细胞数量更多,骨性结合更多,在第4周时即可见成熟骨组织出现,说明补锌能在种植后早期(1-4周)即形成骨性愈合。放射补锌组在第4,12周时也较放射组产生更多骨性结合,说明即使在⁶⁰Co照射后,微量元素锌的补充仍可以促进种植体-骨融合。提示⁶⁰Co照射会延缓种植体骨愈合,放射治疗后适量补锌能够减轻其对种植体骨融合的不利影响。 中国组织工程研究杂志出版内容重点：生物材料;骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性;组织工程     

α-平滑肌肌动蛋白在实验性放射线大鼠肾病组织中的表达和意义

一、材料和方法.1．实验模型建立：按文献[1]的方法制作放射性肾病动物模型。6周雄性Wistar大鼠（日本SLC公司,n=32）被随机分成对照组（n=12）和照射组（n=20）,全麻后开腹将右肾切除,暴露左肾,给予X线25 Gy单次照射。照射后1、3、6、9个月4个时间点分别处死各组动物。     

供体凋亡淋巴细胞预输注对猪肝移植受体CD4+T、CD8+T、CD4+CD25+调节性T细胞的影响

背景：凋亡细胞能够主动调节机体的免疫功能,并能通过调节机体细胞免疫和体液免疫的途径诱导免疫耐受,但这些结果只在大鼠肝脏移植模型中证实。 目的：探讨通过⁶⁰Co γ射线体外处理后的供体淋巴细胞预输注诱导猪肝移植特异性免疫耐受的作用中,对淋巴细胞亚群的影响。 方法：建立非转流小型猪原位肝移植模型。将受体猪随机摸球法均分为2组：空白对照组,受体猪无特殊处理,行肝移植;淋巴细胞组：受体猪在肝移植前7 d经耳静脉注射⁶⁰Co γ射线处理过的5×10⁸个供体淋巴细胞。观察两组受体猪移植后的存活时间,移植后T淋巴细胞亚型CD4⁺T、CD8⁺T、CD4⁺CD25⁺Tr变化及病理。 结果与结论：移植后3 d,两组病理活检均呈急性中、重度排斥反应;移植后6 d,两组均呈急性重度排斥反应。移植后1,3,6 d CD4⁺T、CD8⁺T、CD4⁺CD25⁺Tr升降趋势,两组间差异无显著意义(P > 0.05)。提示,⁶⁰Co γ射线体外处理过的淋巴细胞预输注未能够诱导猪同种异体肝移植特异性免疫耐受,未能引起T淋巴细胞亚群变化有关。     

核磁共振氢谱代谢组学方法确定X射线对小鼠辐射的损伤

背景：单一的血液学分析仅能针对辐射损伤后某个时间点机体的损伤情况,并不能反映机体辐射损伤后的较长期的累积状况。 目的：采用基于核磁共振氢谱的代谢组学研究方法确定X射线对小鼠的辐射损伤后尿液和血液中辐射损伤标志物。 方法：取小鼠48只随机分为4组,分别接受0(假辐射),3,9,27 Gy X射线头部辐射,分别于辐射后24 h和5 d后采血检测。另取小鼠36只随机分为3组,分别接受0(假辐射),9,27 Gy X射线头部辐射,分别于辐射前2 d和辐射后第5天收集24 h尿液检测。采集的血液及尿液进行1H-NMR分析。 结果与结论：接受不同剂量X射线辐射后,血清中天冬氨氨基转移酶和丙氨酸氨基转移酶含量没有显著变化,碱性磷酸酶在9 Gy X射线辐射后有显著性升高,表明低剂量头部辐射可能引起肝脏或者骨骼中辐射损伤修复增加;血清中总超氧化物歧化酶在辐射后第5天出现显著降低,表明小鼠经头部辐射后引起了全身氧化应激效应。尿液中N-乙酰甘氨酸和-胸苷在接受各剂量X射线辐射后均显著升高,可以作为头部辐射后尿液中的辐射损伤标志物。尿液中3-羟基-2-甲基苯甲酸-3-氧硫酸盐在接受9 Gy X射线辐射后升高了2.5倍,可以作为中低剂量辐射损伤的特异标志物;尿液牛磺酸在27 Gy X射线辐射后升高20%,可以作为高剂量辐射损伤的特异标志物。     

20 Gy γ射线不同分割模式头部照射对小鼠学习记忆的影响

目的:探讨20 Gyγ射线不同分割模式头部照射对小鼠学习记忆的影响.方法:48只成年雄性C57BL/6小鼠随机分为对照组(control)、20 Gy单次照射组(20 Gy)、大分割照射组(5 Gy×4 d)和常规分割照射组(2 Gy×10 d),各照射组小鼠均头部接受γ射线照射,总剂量为20 Gy.照后4周采用Mor...     

间充质干细胞可能通过调控免疫细胞促进再生障碍性贫血小鼠骨髓的造血功能

目的:探讨间充质干细胞(MSCs)影响再生障碍性贫血小鼠造血功能的可能免疫机制。方法:30只小鼠分3组,分别为单纯照射组、再障模型组、MSCs治疗组,建立再生障碍性贫血小鼠模型。单纯照射组仅经5Gy[60Co]γ射线照射,再障模型组经5Gy[60Co]γ射线照射后输注DBA/2小鼠胸腺淋巴结细胞1×106cell/只,MSCs治疗组经5Gy[60Co]γ射线照射后输注DBA/2小鼠胸腺淋巴结细胞1×106cell/只,3d后输注人骨髓MSCs1×106cell/只。观察各组小鼠外周血象、骨髓及外周血CD4+细胞、CD8+细胞、CD4+/CD8+、NK细胞变化及与造血的关系。结果:经5Gy[60Co]γ射线照射后,单纯照射组、MSCs治疗组外周血象第7d开始下降,21d血象恢复正常。再障模型组外周血象第7d开始持续性下降,至21d血象仍未恢复。照射后7d,各组小鼠间外周血CD4+细胞、CD8+细胞、CD4+/CD8+无明显差异,但MSCs治疗组NK细胞低于单纯照射组和再障模型组(P0.05)。照射后14d3组CD4+细胞比例均明显下降,CD8+细胞则表现不同,再障模型组与MSCs治疗组CD8+细胞比例明显高于单纯照射组,至照射后21d,MSCs治疗组CD8+、NK细胞与单纯照射组相近、而模型组则明显高于单纯照射组和MSCs治疗组;MSCs治疗组小鼠股骨病理切片中脂肪细胞比例明显低于再障模型组,与单纯照射组结果一致。结论:MSCs输注可能通过调控免疫细胞影响再生障碍性贫血小鼠骨髓造血功能。     

Wistar大鼠的咬肌放射损伤模型

背景：构建稳定可靠的咬肌放射损伤模型对颌面部肿瘤放疗的相关研究有重要意义。 目的：以放射剂量40 Gy照射后Wistar大鼠咬肌构建大鼠咬肌放射损伤模型。 方法：成年Wistar大鼠20只,随机分成正常对照组和放射损伤组。放射损伤组采用直线加速器照射大鼠咬肌区累积40 Gy制造咬肌放射损伤。在28 d后,在光镜及电镜下观察咬肌放射区病理改变,RT-PCR检测转化生长因子β1的基因表达。 结果与结论：40 Gy照射后28 d大鼠咬肌区出现结构受损、血管密度减低(P < 0.01)等放射损伤表现,同时引起转化生长因子β1的基因表达升高(P < 0.001)等机体被动修复表现。结果证实Wistar大鼠咬肌区直线加速器40 Gy照射可以作为咬肌放射损伤模型。     

不同生长期小鼠胸腺T细胞不同亚群的变化及ROCK抑制剂对衰老小鼠胸腺再生的促进作用

目的研究各发育阶段小鼠胸腺细胞、胸腺上皮细胞(TEC)和脾脏中T细胞的变化,探索Rho相关卷曲蛋白激酶(ROCK)抑制剂对衰老小鼠胸腺再生的作用。方法取幼年、青年、中年及老年期C57BL/6雌鼠的胸腺和脾脏,流式细胞术分析小鼠胸腺细胞、TEC及脾脏中T细胞亚群;ROCK抑制剂体外处理衰老进程中小鼠TEC,荧光酶联斑点分析仪观察细胞增殖情况;ROCK抑制剂处理20月龄衰老小鼠,流式细胞术检测小鼠胸腺细胞、TEC及脾脏中T细胞亚群的变化。结果随月龄增加,胸腺细胞、TEC总数及各细胞亚群数量均显著降低;脾脏中总CD4⁺T细胞及CD8⁺T细胞比例无显著性改变,但CD4+初始T细胞、CD8+初始T细胞和CD4+近期胸腺迁出细胞(RTE)在脾脏中所占比例呈下降趋势;ROCK抑制剂在体外促进衰老进程中小鼠TEC增殖,ROCK抑制剂在体内使衰老小鼠胸腺细胞、TEC以及外周脾脏中T淋巴细胞各亚群数量明显增加。结论随着小鼠月龄增加,胸腺呈进行性退化。ROCK抑制剂可以显著缓解衰老小鼠胸腺的萎缩,促进衰老小鼠胸腺再生。     

Sequential appearance of T-cell receptor gamma delta- and alpha beta-bearing intestinal intra-epithelial lymphocytes in mice after irradiation.

We have previously reported that T-cell receptor (TcR) gamma delta-bearing T cells precede TcR alpha beta-bearing T cells in appearance in the thymus after whole-body irradiation. In the present study, the kinetics of appearance of intestinal intra-epithelial lymphocytes (IEL) was examined in mice after whole-body irradiation with a lethal dose of 9.5 Gy or with a sublethal dose of 6 Gy. The number of CD3+ IEL decreased to the lowest value 4 days after irradiation with 9.5 Gy, and thereafter increased to half as many as the normal level by day 7. Thy-1+TcR alpha beta- IEL and Thy-TcR alpha beta- IEL recovered considerably by day 7 after the irradiation, whereas Thy-1+TcR alpha beta+ IEL and Thy-1+TcR alpha beta+ IEL hardly recovered at this stage. All mice died within 12 days after irradiation with a lethal dose of 9.5 Gy. On the other hand, when irradiation dose was decreased to 6 Gy, all mice survived beyond 40 days after irradiation. The number of CD3+ IEL recovered to the normal level by 10 days after irradiation with 6 Gy. Consistently with the results in mice irradiated with a lethal dose, the first cells to increase in IEL of mice irradiated with a sublethal dose were TcR gamma delta+ IEL expressing Thy-1 antigen. The number of Thy-1+TcR gamma delta+ IEL increased to approximately two-fold as many as that in normal mice by day 10, while TcR alpha beta+ IEL began to increase in number from day 20 after irradiation and recovered to the normal level by day 40 after irradiation. Thus, sequential appearance of TcR gamma delta+ and TcR alpha beta+ IEL was evident after irradiation, similar to that seen in the thymus after irradiation. The IEL on day 10 after a sublethal irradiation, which is composed mainly of Thy-1+TcR gamma delta+ IEL, exhibited a strong cytolytic activity against P815 in the presence of anti-CD3 mAb, suggesting that the early appearing Thy-1+TcR gamma delta+ IEL may play important roles in epithelial immunity at an early stage after irradiation.     

Evaluation of the radioprotective effect of Liv 52 in mice

Liv 52 is a mixture of botanicals that is used clinically to treat various hepatic disorders. In this study, the radioprotective activity of Liv 52 was evaluated in mice given whole-body exposure to different doses of gamma-radiation. In addition, a series of studies was conducted to explore the mechanism of radioprotection. Radioprotection was evaluated by the ability of Liv 52 to reduce both the frequency of bone marrow micronucleated erythrocytes and the lethality produced by (60)Co gamma-radiation. Mice were treated by oral gavage once daily for seven consecutive days with 500 mg/kg body weight Liv 52 or carboxymethylcellulose vehicle prior to radiation. Micronucleated polychromatic erythrocytes (MPCEs), micronucleated normochromatic erythrocytes (MNCEs), and the PCE/NCE ratio were measured at 0.25-14 days after exposure to whole-body radiation doses of 0, 0.5, 1.5, 3.0, or 4.5 Gy; animal survival was monitored after doses of 7, 8, 9, 10, 11, or 12 Gy. Pretreatment of mice with Liv 52 significantly reduced the frequency of radiation-induced MPCEs and MNCEs. Irradiation reduced the PCE/NCE ratio in a dose-related manner for up to 7 days following irradiation; Liv 52 pretreatment significantly mitigated against these reductions. Liv 52 treatment also reduced the symptoms of radiation sickness and increased mouse survival 10 and 30 days after irradiation. Liv 52 pretreatment elevated the levels of reduced glutathione (GSH), increased the activities of glutathione transferase, GSH peroxidase, GSH reductase, superoxide dismutase, and catalase, and lowered lipid peroxidation (LPx) and the activities of alanine amino transferase and aspartate aminotransferase 30 min after exposure to 7 Gy of gamma-radiation. Liv 52 pretreatment also reduced radiation-induced LPx and increased GSH concentration 31 days following the exposure. The results of this study indicate that pretreatment with Liv 52 reduces the genotoxic and lethal effects of gamma-irradiation in mice and suggest that this radioprotection may be afforded by reducing the toxic effects of the oxidative products of irradiation.     

TLR在小鼠胸腺中的表达及其在胸腺细胞发育中的可能作用

检测体外培养和体内发育过程中,胎鼠胸腺处于不同发育阶段时Toll样受体(TLR)的表达,阐明TLR表达量与胸腺细胞发育相关性,为TLR和胸腺细胞发育分化相关研究提供基础数据。无菌取15d胎龄胎鼠胸腺进行体外培养(FTOC),在培养不同时间点(2d,4d,6d),检测处于不同发育期胸腺TLR的表达;同时在孕期不同天数(15~19d),分别取胎鼠胸腺,检测在体内发育过程中胸腺TLR的表达;在FTOC中加入二脱氧鸟苷培养6d以制备胸腺基质细胞,检测基质细胞与胸腺细胞TLR表达情况。结果:小鼠胸腺中检测到多种TLR。FTOC培养中:培养第2天(F2)开始检测到各种TLR,到培养第6天(F6),TLR1,TLR3,TLR6,TLR7,TLR8明显上调,而TLR4,TLR5保持低水平,TLR4在培养第6天又下降;体内发育过程中:TLR6表达量随胎龄增加有较明显上调,TLR1,TLR3-8保持低水平表达;TLR2,TLR9体内体外都未检测到明显表达。在对胸腺细胞与基质细胞TLR表达比较中发现TLR1,TLR5,TLR6,TLR7高表达于胸腺细胞。胎鼠胸腺表达某些TLR,并且在发育不同阶段表达量有所改变,提示TLR可能参与胸腺细胞的发育过程。     

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。     

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.     

Target cells of apoptosis in the adult murine dentate gyrus and O4 immunoreactivity after ionizing radiation

The occurrence of radiation-induced apoptosis and the determination of target cells were investigated by using the TdT-mediated dUTP-biotin nick end labeling assay and immunohistochemical analyses. The O4 immunoreactivity, an oligodendrocytes surface antigen, was also evaluated by using western blotting analysis. C57BL/6J adult female mice were subjected to single dose irradiation of 10 Gy. Eight hours after irradiation, the most significant increase of apoptotic cells was detected in the subgranular zone and the hilus of the dentate gyrus. The target cells of radiation-induced apoptosis are the subgranular progenitor cells and the oligodendrocytes in the hilus. The amount of the O4 immunoreactivity, a marker for premature oligodendrocytes, was unchanged until 8 h but enhanced after 12 h of irradiation. These results are the first to show the increase of the O4 immunoreactivity after irradiation and may be associated with the pathogenesis of radiation injury.