奈达铂体外诱导肺腺癌A549细胞凋亡及其作用机制

目的探讨奈达铂(NDP)体外对人肺腺癌A549细胞的影响及其作用机制。方法采用四氮甲唑蓝(MTT)比色法检测不同浓度的NDP对A549细胞的杀伤作用,计算半数抑制浓度(IC50);流式细胞术(FCM)测定给药前后细胞凋亡率及周期分布变化;半定量PCR分析凋亡基因Bax、Caspase-3、Caspase-9的表达情况。结果 NDP能显著抑制A549细胞的生长;FCM结果显示,10μg/mL NDP作用A549细胞48h后,与对照组相比,细胞凋亡明显增加[(25.14±3.97)%vs.(8.01±1.46)%];S期细胞的比例增加[(52.73±1.66)%vs.(38.38±3.91)%],差异均有统计学意义(P<0.05)。与对照组相比,Bax、Caspase-3、Caspase-9表达增加(P<0.05)。结论 NDP可抑制A549细胞增殖,其机制可能与诱导细胞凋亡、细胞S期阻滞及上调Bax、Caspase-3和Caspase-9的表达有关。     

四味芳香开窍药的挥发性成分对缺血缺氧PC12细胞及细胞内Ca2+的影响

目的研究四味芳香开窍药的挥发性成分对连二亚硫酸钠(Na2S2O4)致PC12细胞缺血缺氧损伤及细胞内Ca2+的影响。方法体外实验采用5mmol/L的Na2S2O4导致PC12细胞缺血缺氧性损伤,然后观测细胞形态;用二甲基噻唑二苯基四唑溴盐(MTT)比色法,考察水蒸汽蒸馏法提取的麝香、苏合香、安息香挥发性成分及冰片对缺血缺氧PC12细胞活性的影响;并按照试剂盒要求测定模型细胞内Ca2+的含量。结果麝香4、8、16μg/mL,冰片8、16μg/mL,苏合香20、40μg/mL及安息香16μg/mL组均能显著升高模型细胞的吸光度(A)值(P<0.05,P<0.01),显著抑制Na2S2O4对PC12细胞的损伤;苏合香40、80μg/mL,安息香4、8、16μg/mL组均能显著降低模型细胞内Ca2+含量(P<0.05,P<0.01);麝香、冰片有降低模型细胞内Ca2+含量的趋势。结论麝香、苏合香、安息香的挥发性成分及冰片均有保护缺血缺氧PC12细胞的作用,其机制可能与降低细胞内Ca2+的含量,防止钙超载有关。     

大黄素对模拟冷缺血再灌注后肝细胞内钙离子浓度及细胞凋亡的影响

目的 研究中药大黄素对模拟冷缺血再灌注后肝细胞内钙离子浓度及细胞凋亡的影响.方法 体外培养肝细胞株HL-7702,随机分为对照组和大黄素处理组.对照组未予大黄素处理,大黄素处理组按100、10、1 μmol/L分为高、中、低3个浓度组,建立模拟冷缺血再灌注模型,流式细胞技术检测各组细胞内钙离子浓度及细胞凋亡水平,分别检测各组细胞培养上清液乳酸脱氢酶水平.结果 冷缺血8 h再灌注6 h后,高、中、低浓度大黄素处理组钙离子荧光强度分别为(24.12±0.51)、(26.35±1.34)、(39.12±1.94),均显著低于对照组的105.29±1.01(P<0.01).高、中、低浓度大黄素处理组细胞凋亡率分别为(5.46±0.41)%、(10.64±0.64)%、(11.90±0.50)%,均显著低于对照组的(25.40±1.41)%(P<0.01).高、中浓度大黄素处理组上清液LDH含量分别为(179.67±18.57)u/L、(198.83±14.22)u/L,显著低于对照组的(351.33±34.16)u/L(P<0.01).结论 大黄素可降低模拟冷缺血再灌注后的肝细胞内钙离子浓度,抑制细胞凋亡,减轻肝细胞损伤.     

紫杉醇诱导人肺腺癌多药耐药细胞系的建立及DNA polβ、mdr1、mrp1、GST-πl、rp和topo Ⅱ基因的表达

目的体外建立人肺腺癌细胞多药耐药细胞系,观察其生物学特性并探讨其细胞内DNA polβ和多药耐药基因mdr1、mrp1、GST-πl、rp和topo Ⅱ的表达及意义。方法以紫杉醇为诱导药,采用间歇逐步增加剂量法建立人肺腺癌多药耐药细胞系A549/TXL20;MTT法检测A549/TXL20对紫杉醇、顺铂、长春新碱、5-氟尿嘧啶和丝裂霉素的耐药指数(RF);细胞克隆形成法测定A549/TXL20对紫杉醇的敏感性;高效液相色谱测定细胞内紫杉醇的浓度;RT-PCR法测定人肺腺癌多药耐药细胞系A549/TXL20中DNA polβ、mdr1、GST-π、mrp1l、rp和topo Ⅱ的基因表达。结果①A549/TXL20形态不规则,较亲本细胞略小,核/浆比增加,倍增时间没有明显变化;②A549/TXL20对紫杉醇的RF为19.3,对顺铂的RF为67.4,对长春新碱、5-氟尿嘧啶、丝裂霉素和顺铂等抗癌药物有不同程度的耐药性;③A549/TXL20对紫杉醇的敏感性降低,其紫杉醇的含量较亲本细胞下降;④A549/TXL20细胞中DNA polβ、mdr1、GST-π、mrp1l、rp的基因表达量分别较A549细胞中的表达量明显增加,差异具有统计学意义(P<0.05)。结论建立了相对稳定的人肺腺癌多药耐药细胞系A549/TXL20,其耐药机制可能与mdr1、GST-π、mrp1l、rp和DNA polβ基因的高表达有关。     

蛋白酶活化受体-1单克隆抗体的制备与鉴定

目的制备蛋白酶活化受体-1(PAR-1)单克隆抗体(mAb)。方法以PAR-1特异性片段为免疫原(13肽)免疫BALB/c小鼠,运用杂交瘤技术制备抗PAR-1 mAb。采用捕获酶联免疫吸附试验(capture ELISA)鉴定mAb的Ig亚类;通过ELISA、Dot blot、免疫组化染色法、流式细胞仪分析、激光共聚焦显微镜技术鉴定mAb的特异性。结果获得2株可稳定分泌抗PAR-1 mAb的杂交瘤细胞,其亚型分别为IgMI、gG2b。免疫组化染色表明,mAb与人扁桃体、结肠组织中的淋巴细胞、包皮组织中的成纤维细胞、肺组织中的巨噬细胞反应呈阳性。流式细胞仪分析显示,2株mAb与人肺腺癌细胞系A549细胞胞浆内及细胞膜上的PAR-1均呈阳性反应。激光共聚焦扫描显微镜观察,荧光标记的阳性反应物在A549细胞胞浆内及细胞膜上均可见。结论成功地制备出抗PAR-1 mAb,为进一步研究炎症性疾病提供有用的试剂。     

T-2毒素对胎儿软骨细胞凋亡、Bcl-2和Bax表达的影响及硒的保护作用

目的　探讨T 2毒素对软骨细胞凋亡的作用,和对凋亡调控蛋白Bcl 2 与Bax表达的影响,以及微量元素硒对软骨细胞的保护作用。方法　采用电镜,Annexin V/PI法检测T 2 毒素致人软骨细胞凋亡的情况,采用流式细胞仪检测凋亡相关蛋白Bcl 2和Bax的表达。结果　T 2 毒素可引起软骨细胞发生凋亡的典型电镜形态改变;不同浓度(1~20μg/L)的T 2毒素均可以引起软骨细胞早期凋亡率和晚期凋亡率明显增加,且在一定范围内呈浓度依赖性,T 2毒素浓度为20μg/L时早期凋亡率最高达5.60%,晚期凋亡率最高达8.61%。生理浓度的微量元素硒可部分减弱T 2毒素引起的凋亡;不同浓度(1~20μg/L)的T 2毒素都能引起Bcl 2和Bax表达水平提高,浓度为10~20μg/L时,Bax/Bcl 2比值升高;硒能部分对抗T 2 毒素引起的Bcl 2 和Bax 表达的提高,使Bax/Bcl 2 比值下降,以降低凋亡率。结论　T 2毒素在浓度为1 ~ 20μg/L 时,可以引起软骨细胞凋亡; T 2 毒素引起的软骨细胞凋亡与软骨细胞内Bax/Bcl 2比值升高有关,硒对T 2毒素引起的软骨细胞凋亡有一定保护作用。     

β-榄香烯对肾癌细胞的体外放射增敏作用

目的　探讨 β 榄香烯对肾癌细胞GRC 1的体外放射增敏作用及机理。 方法　将GRC 1细胞分为空白组 (加培养液 2mL)、空白乳组 (加空白乳培养液 2mL)和加药组 (加 5 0mg·L -1榄香烯乳培养液 2mL) ,培养 2 4h后 ,3组细胞悬液在剂量率 4 0 0cGy·min-1时 ,分别接受来自 6MeV直线加速器不同剂量的x线照射。计数被照细胞克隆群数 ,绘制细胞放射 存活曲线图。流式细胞仪检测各组细胞的周期变化与凋亡。对 3组爬片细胞进行免疫细胞化学染色 ,成像系统灰度分析bcl 2与PCNA基因表达。结果　流式细胞术显示 ,5 0mg·L -1榄香烯乳对肾癌细胞的G2 M阻滞作用随时间增加而增强 ,2 4h时作用达高峰 ;随时间和照射剂量的增加细胞凋亡水平增高。细胞爬片的成像系统灰度分析显示加药组与空白组相比 ,bcl 2基因表达降低 2 0 % ,而两组PCNA无表达。结论　β 榄香烯乳对肾癌细胞GRC 1有放射增敏作用 ,其作用机制可能与下调bcl 2基因表达 ,诱导GRC 1细胞凋亡和对细胞G2 M期阻滞有关     

Induction of apoptosis and inhibition of proliferation of C6 glioma cells in vitro by tamoxifen

Objective To investigate the anti-tumor effect and mechanism of tamoxifen on rat C6 glioma cells. Methods C6 cells were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） with 3% fetal calf serum （FCS）, and treated with tamoxifen of different concentrations, i.e. group A （1.25 μmol/L）, group B （2.50 μmol/L）, group C （5. 00 μmol/L）, group D （10. 00 μmol/L）, group E （20. 00 μmol/L） and control group （0. 00 μmol/L）. Morphological changes, MTT assay and 5-bromo-2＇-deoxyuriding labeling ratio were assessed. Apoptosis was observed by flow cytometry. Results C6 cells treated with different doses of tamoxifen for 24, 48, and 72 hours became irregular in shape, while cells treated with vehicle grew normally. MTT assay showed that tamoxifen did not suppress C6 cell growth until 72 hours after treatment. Seventy-two hours after treatment, there were significant differences in cell viable rate between group A versus groups C, D and E; so did group B versus group D as well as group E （P〈 0.05 ）. BrdU incorporation assay indicated significant difference of BrdU labbled index （BrdU LI） among groups A, C, E and control group 48 hoers after treatment （P〈0.05）. And the BrdU LI decreased with the increased concentration of tamoxifen. Flow cytometry （FCM） showed significant difference between treated group and control group at 24, 48, and 72 hours after treatment （P〈0.05）. Conclusion Tamoxifen significantly suppresses the growth of C6 glioma cells in a time- and dose-dependent manner. The mechanism of tamoxifen suppressing C6 glioma cells may be inhibiting proliferation and inducing apoptosis. Therefore, tamoxifen can be a candidate as a chemotherapy agent for glioma.     

Effects of Panax notoginseng saponins on hydrogen peroxide-induced apoptosis in cultured rabbit bone marrow stromal cells

Objective To investigate the effects of Panax notoginseng saponins (PNS) on hydrogen peroxide (H2O2)-induced apoptosis in cultured rabbit bone marrow stromal cells (BMSCs). Methods BMSCs from 3-month-old New Zealand rabbits were isolated and cultured by the density gradient centrifugation combined with adherent method. The cultured BMSCs were divided into three groups: normal control, H2O2 treatment (100μmol/L), and PNS pretreatment (0.1g/L). Intracellular reactive oxygen species (ROS) levels as the index of oxidative stress were measured by using 2'7'-dichlorodihydrofluorescein diacetate. Flow cytometry was used to observe the apoptosis of BMSCs by staining with annexinV-FITC/PI. The protein expression of Bax in BMSCs was analyzed by Western blotting. Activity of caspase-3 enzyme was measured by spectrofluorometry. Results Pretreatment with PNS significantly decreased intracellular ROS level induced by H2O2 (P<0.01). PNS markedly attenuated H2O2-induced apoptosis rate from 38.68% to 19.24%(P<0.01). PNS reversed H2O2-induced augmentation of Bax expression. Furthermore, PNS markedly reduced the altered in activity of caspase-3 enzyme induced by H2O2(P<0.01). Conclusion PNS has a protective effect on hydrogen peroxide-induced apoptosis in cultured rabbit BMSCs by scavenging ROS and decreasing Bax expression and caspase-3 activity.     

环氧化酶-2及表皮生长因子受体在非小细胞肺癌组织中的表达及临床意义

目的探讨环氧化酶-2(COX-2)与表皮生长因子受体(EGFR)在非小细胞肺癌(NSCLC)组织中的表达及与肺癌发生发展的关系。方法采用免疫组化(SP)法检测56例NSCLC和20例正常肺组织中COX-2与EGFR的表达。结果56例NSCLC组织中,COX-2与EGFR表达阳性率分别为64.2%和67.8%,显著高于正常肺组织(P<0.01),COX-2与EGFR表达与临床分期、病理分级、组织学分型和淋巴结转移密切相关(P<0.05),肿瘤分期愈晚,细胞分化越差,淋巴结转移越高,COX-2与EGFR表达阳性率越高,腺癌中COX-2表达明显高于鳞癌,鳞癌中EGFR表达高于腺癌(P<0.05)。结论COX-2与EGFR在NSCLC中异常表达说明其在肺癌发生发展中有重要作用,可作为判断NSCLC的生物学行为及估计预后的指标。     

Study of the mechanism on the apoptosis induced in Human leukemia cell line K562 by the combination of indole-3-acetic acid and horseradish peroxidase

Objective To investigate the mechanisms of apoptosis induced in Human leukemia cell line K562 by the combination of indole-3-acetic acid and horseradish peroxidase. Methods Human leukemia cell line K562 were exposed to indole-3-acetic acid （IAA） at 20, 40, 60, 80 or 100 mol/L and horseradish peroxidase（HRP） at 1.2 g/mL for varying times. MTT assay was applied to detect the cell proliferation. Flow cytometry was performed to detect the arrest of cell cycle. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assay was used to measure apoptosis. 2, 7-dichlorofluorescin diacetate （DCFH-DA） uptake was measured to determine free radical by confocal microscope. Content of malondiadehyde （MDA） and activity of superoxide dismutase （SOD） were measured by biochemical methods. Results IAA/HRP initiated growth inhibition of K562 cells in a dose- and time-dependent manner. Flow cytometry revealed that cell cycle arrested at G1/G0 after 24 hours treatment. After 72 hours treatment, apoptotic rate of 100 mol/L IAA group increased to 43.9 %, which was 5 times that of control（P〈0.01）. Content of MDA and activity of SOD increased respectively in treatments compared with control. Meanwhile, IAA/HRP stimulated the formation of free radical, which was increased by IAA concentration-dependently. Conclusion The combination of IAAand HRP can inhibit the growth of Human leukemia cell line K562 in vitro by inducing apoptosis which is associated with the increase of free radical. The combination of IAA and HRP might be a promising chemopreventive and chemotherapeutic agent against human leukemia.     

ANTITUMOR MECHANISM OF GEM10 BY THE NATURAL KILLER ACTIVITY AND INTERLEUKIN-2 PRODUCTION

Studiesongermaniumcompoundsshowedthattheyhavemanybiologicaleffects ,suchasanti tu mor[1] ,improvingimmunity[2 ] ,reducingthecon centrationofbloodcholestrolandtrilycerides[3] ,in hibitingvirusreproduction ,butthesideeffectsoftoxicrestricttheirclinicaluses[4 ,5] .Therefore ,itisstillnecessarytodevelopothernewcompoundsoforganogermaniums.GeM 10 ,aneworganicgerma niumcompounds alkili metalcomplexcombinedwitheffectiveextractsofsomeChinesetraditionalherbs ,hasbeendemonstratedtobesaferandmorereliable.…     

苯妥英钠对大鼠牙龈上皮细胞增殖和凋亡的影响

目的观察苯妥英钠(PHT)对大鼠牙龈上皮细胞增殖和凋亡的影响。方法将60只雄性SD大鼠随机分为5组:对照组(腹腔注射灭菌生理盐水1mL)和0、5、25、50、100mg/mL PHT组(腹腔注射上述质量浓度PHT),连续28d;监测PHT血药浓度;29d处死大鼠,制作牙龈组织切片,采用原位脱氧核糖核苷酸末端标记法(TUNEL)检测牙龈上皮细胞的凋亡情况;采用免疫组织化学方法检测牙龈上皮细胞Ki-67的表达。结果实验组凋亡指数(AI)显著低于对照组(P<0.01),而增殖指数(PI)显著高于对照组(P<0.01);PHT血药浓度与AI呈显著负相关(r=-0.98),与PI呈显著正相关(r=0.976)。结论 PHT通过抑制牙龈上皮细胞凋亡和促进细胞增殖,导致牙龈上皮的增生;PHT血药浓度与增生程度可能存在关联。     

γ-射线诱导HL-60细胞凋亡的观察

目的 观察γ-射线诱导HL-60细胞凋亡的时间和剂量效应,以探求辐射诱发肿瘤细胞凋亡分子机制。方法 分别以2.5、5、7.5、10、15Gy γ射线照射HL60细胞,于照后继续培养3、6、9、12、24、27、30h,分别收获细胞。电泳检测DNA梯状带;流式细胞术(FCM)细胞凋亡定量并观察细胞周期变化;Hoechst 33258-PI复染荧光显微镜计数凋亡细胞及已死亡细胞百分率。结果 HL-60细胞受照后死亡方式主要是凋亡,其首先阻滞在G２／M期并由此走向凋亡;DNA梯状带及FCM检测结果发现,细胞凋亡具有时间和剂量依赖性;Hoechst 33258PI染色法检测结果与FCM检测的凋亡细胞随剂量的加大及时间的推移而增多的结果并不呈平行关系。结论 γ-射线诱导HL-60细胞凋亡时间和剂量效应关系的确立为进一步探讨该凋亡途径分子机制奠定了基础。     

雷公藤内酯醇抑制牛晶状体上皮细胞增殖

目的探讨雷公藤内酯醇(Triptolide,Tri)对体外培养的牛晶状体上皮细胞(bovine Lens epithelial cell,BLECs)增殖的抑制作用。方法取第4代对数生长期的牛LECs,培养24 h后,加入重组人表皮生长因子(recombi-nant human epithelial growth factor,rhEGF)(终浓度50μg/L)和不同浓度的Tri(40、20、10μg/L),再分别作用6、12、24、48、72 h后,采用MTT法及流式细胞仪检测增殖细胞核抗原(PCNA)在LECs的阳性表达率和增殖抑制率,观察Tri对LECs增殖的抑制作用。结果不同浓度Tri均可抑制处于增殖状态的LECs,并呈剂量和时间依赖性;72 h增殖抑制率分别达到80.09%、61.29%及39.93%。PCNA表达率在6-72 h内随浓度增高和作用时间延长有明显的下调,呈明显的时间-效应关系和剂量-效应关系,且各浓度Tri组与同一时点增殖对照组相比均有非常显著性差异(P<0.01)。结论Tri对牛晶状体上皮细胞增殖有明显的抑制作用。     

光动力疗法对人乳腺癌细胞MDA-MB-231凋亡的影响

目的探讨光动力疗法(PDT)对人乳腺癌细胞凋亡的影响。方法以人乳腺癌细胞株MDA-MB-231为研究对象,以血卟啉衍生物(HpD)为光敏剂,以630 nm波长激光为光源,采用连续照射的方式。将不同浓度HpD染色的MDA-MB-231细胞,照射不同剂量的激光后,用MTT法测定其A492值,选择最佳作用参数;电镜观察PDT作用后不同时间的细胞凋亡情况,并采用免疫组化方法检测促凋亡蛋白Bax和抗凋亡蛋白Bcl-2的表达情况。结果随着PDT作用后时间的延长,细胞凋亡现象越明显;Bax蛋白表达无明显变化(P>0.05),而Bcl-2蛋白表达自PDT后6 h起显著下降(P<0.01),PDT后6 h Bax/Bcl-2比值依次递增,且有统计学意义(P<0.05)。结论光动力疗法可诱导人乳腺癌细胞发生凋亡,其机制可能与Bax和Bcl-2蛋白表达的比值有关。     

白藜芦醇对大鼠重症急性胰腺炎肠黏膜细胞凋亡的影响

目的探讨白藜芦醇对试验性大鼠重症急性胰腺炎肠黏膜细胞凋亡及凋亡调控基因Bax蛋白表达的影响。方法54只成年雄性SD大鼠随机分为假手术组(sham operation group,SO)、模型组(severe acute pancreatitis,SAP)、治疗组(resveratrol-treated group,RES)。假手术组于开腹翻动十二指肠后关腹,模型组以40 g/L牛磺胆酸钠1 mL/kg胰胆管逆行注射制造重症急性胰腺炎模型。治疗组制模后立即于阴茎背静脉注射等剂量白藜芦醇(5 mg/mL1、0 mg/kg)。于3、61、2 h 3个时间点各剖杀6只大鼠。TUNEL法检测肠黏膜上皮细胞凋亡,免疫组化法检测小肠组织中Bax蛋白的表达。结果治疗组3、6、12 h肠黏膜细胞凋亡指数明显低于模型组(P<0.01)。治疗组各时间点Bax蛋白表达阳性率显著低于模型组(P<0.01)。结论白藜芦醇可通过抑制肠黏膜上皮细胞的凋亡,维持肠黏膜屏障的完整性,从而防止了急性重症胰腺炎细菌和毒素的移居。     

平阳霉素局部注射对鼻息肉病息肉组织病理学的影响

目的通过观察平阳霉素治疗前后鼻息肉病息肉组织的病理变化情况,探讨平阳霉素治疗鼻息肉病的机制。方法应用末端脱氧核苷酸转移酶介导的脱氧三磷酸尿苷缺口末端标记法(TUNEL法)检测凋亡细胞,与相邻连续的HE染色片对位对照观察嗜酸性粒细胞的凋亡情况。结果平阳霉素治疗前鼻息肉组织嗜酸性粒细胞表达显著高于正常下鼻甲(P<0.01);治疗后鼻息肉组织中的嗜酸性粒细胞表达明显低于治疗前(P<0.01);治疗后鼻息肉组织中嗜酸性粒细胞的凋亡指数高于治疗前(P<0.01)。结论嗜酸性粒细胞是鼻息肉病息肉组织中主要的浸润炎细胞;平阳霉素可通过促进嗜酸性粒细胞凋亡达到治疗鼻息肉病的目的。     

Aβ诱导PC-12细胞凋亡建立阿尔茨海默病细胞模型

目的　用β 淀粉样蛋白 (Aβ2 5- 35)诱导PC 1 2细胞凋亡以建立阿尔茨海默病细胞模型。方法　体外培养大鼠嗜铬细胞瘤PC 1 2细胞 ,以不同浓度Aβ2 5 - 35诱导并于不同时间收获细胞 ,应用MTT法观察细胞活力 ,Fura 2 /AM荧光分析法检测细胞内游离Ca2 +浓度 ,Hoechst332 5 8及碘化丙啶复染分析细胞凋亡。结果　Aβ2 5- 35作用于PC 1 2细胞后 ,细胞活力逐渐下降 ,并呈时间和剂量依赖性 ;同时细胞内Ca2 +浓度显著上升 ;不同浓度Aβ2 5 - 35作用后 ,PC 1 2细胞于不同时间出现凋亡的典型形态学特征 ,该时间比Ca2 +浓度上升约晚 6～ 1 2h。结论　Aβ2 5- 35诱导后PC 1 2细胞活力下降、细胞内Ca2 +浓度上升及细胞凋亡 ,可作为较理想的阿尔茨海默病细胞模型     

EFFECTS OF ANTISENSE OLIGODEOXYNUCLEOTIDES ON EXPRESSION OF CASPASE-3 IN Γ-RADIATION INDUCED APOPTOTIC HL-60 CELLS

Objective To study the inhibitory effects of caspase-3 mRNA antisense oligodeoxynucleotides (ASODN) on expressions of caspase-3 and it's mRNA in γ-radiation induced apoptotic HL-60 cells, and screen the effective ASODN. Methods ASODN-1 and ASODN-2 targeting 5′-noncoding region and initial translation region of caspase-3 mRNA were respectively designed, synthesized and introduced into HL-60 cells by means of liposome-mediated transfection followed by 10Gy γ-radiation exposures. TUNEL assay was conducted to investigate the morphologic change and apoptotic percentage of HL-60 cells 18 h later. Immunocytochemical staining and one step RT-PCR were respectively performed to detect the expressions of caspase-3 and it's mRNA. Mismatched oligodeoxynucleotide (MODN) transfected and un-transfected HL-60 cells were taken as control. Results TUNEL assay found that the apoptotic percentages in ASODN-1 and ASODN-2 groups were significantly reduced compared with the control groups (P<0.01) when the final concentration of both ASODNs was ≥3μmol/L. Immunocytochemistry showed that caspase-3 positive cell percentages were reduced but the average gray values increased significantly compared with the control groups (P<0.01). RT-PCR showed expressions of caspase-3 mRNA was decreased after ASODN transfection. Furthermore, ASODN-1 proved more effective in inhibiting HL-60 cell apoptosis than ASODN-2 (P<0.01). Conclusion Caspase-3 mRNA ASODNs can prevent HL-60 cells from apoptosis induced by γ-radiation and reduce expression of caspase-3 and its mRNA. These effects are dose dependent in a certain range.