姜黄素对放射性血管内皮损伤的保护作用

目的 探讨姜黄素对放射性血管内皮损伤的保护作用及其机制.方法 对人脐静脉内皮细胞(HUVEC)分离培养后分组,以2、4、6和8Gy4种不同剂量进行β线照射,并设未照射组为对照.分别通过光学显微镜及电子显微镜观察细胞形态和超微结构改变;流式细胞仪法观察各组的凋亡率和坏死率以及细胞内活性氧(ROS)生成;检测细胞照射前后乳酸脱氢酶(LDH)活力和丙二醛(MDA)含量的变化.结果 细胞经照射后,形态及超微结构改变均显示为典型的凋亡改变,而姜黄素预处理组的细胞凋亡率和坏死率均明显轻于其他实验组,差别有统计学意义(P＜0.05).LDH活力和MDA含量在各照射组均高于姜黄素预处理组(P＜0.05),照射后各组ROS含量明显升高,呈剂量依赖性改变,明显高于姜黄素预处理组,差别均有统计学意义(P＜0.05).结论 放射线照射可导致HUVEC凋亡和坏死,细胞内LDH活力和MDA含量增高,且呈剂量依赖性.姜黄素对受照射后的HUVEC凋亡和坏死有保护作用.     

不同剂量电离辐射对大肠癌HCT-8细胞P-gp表达的影响

目的 通过检测不同剂量电离辐射对大肠癌细胞多药耐药基因MDR1的蛋白表达产物P-糖蛋白(P-gp)的影响,探讨逆转肿瘤多药耐药的方法。方法 采用流式细胞术检测P-gp蛋白表达的变化。结果 与假照组相比,2Gy大剂量照射后P-gp阳性细胞百分率明显增加(P<0.01),先给予低剂量照射(0.05Gy,0.1Gy)后,再给予大剂量照射,P-gp阳性细胞百分率亦有明显增加(P<0.05),0.2Gy+2Gy组P-gp阳性细胞百分率明显增加(P<0.01)。与单纯2Gy大剂量照射组比较,0.1Gy+2Gy组P-gp阳性细胞百分率明显降低(P<0.05)。结论 低剂量辐射可以逆转大剂量辐射所致的多药耐药性。     

Mitochondria-targeted superoxide dismutase (SOD2) regulates radiation resistance and radiation stress response in HeLa cells

Reactive oxygen species (ROS) act as a mediator of ionizing radiation-induced cellular damage. Previous studies have indicated that MnSOD (SOD2) plays a critical role in protection against ionizing radiation in mammalian cells. In this study, we constructed two types of stable HeLa cell lines overexpressing SOD2, HeLa S3/SOD2 and T-REx HeLa/SOD2, to elucidate the mechanisms underlying the protection against radiation by SOD2. SOD2 overexpression in mitochondria enhanced the survival of HeLa S3 and T-REx HeLa cells following γ-irradiation. The levels of γH2AX significantly decreased in HeLa S3/SOD2 and T-REx HeLa/SOD2 cells compared with those in the control cells. MitoSox(TM) Red assays showed that both lines of SOD2-expressing cells showed suppression of the superoxide generation in mitochondria. Furthermore, flow cytometry with a fluorescent probe (2',7'-dichlorofluorescein) revealed that the cellular levels of ROS increased in HeLa S3 cells during post-irradiation incubation, but the increase was markedly attenuated in HeLa S3/SOD2 cells. DNA microarray analysis revealed that, of 47,000 probe sets analyzed, 117 and 166 probes showed more than 2-fold changes after 5.5 Gy of γ-irradiation in control and HeLa S3/SOD2 cells, respectively. Pathway analysis revealed different expression profiles in irradiated control cells and irradiated SOD2-overexpressing cells. These results indicate that SOD2 protects HeLa cells against cellular effects of γ-rays through suppressing oxidative stress in irradiated cells caused by ROS generated in the mitochondria and through regulating the expression of genes which play a critical role in protection against ionizing radiation.     

茶多酚对ox-LDL诱导人脐静脉内皮细胞凋亡的抑制作用

目的:探讨茶多酚(teapolyphenols,TP)对氧化型低密度脂蛋白(oxidizedlowdensitylipoprotein,ox-LDL)诱导人脐静脉内皮细胞(humanumbilicalveinendothelialcell,HUVEC)凋亡的抑制作用及其机制。方法:实验分为四组:TP(25μg/ml)组、ox-LDL(200μg/ml)+TP(25μg/ml)组、ox-LDL(200μg/ml)组、对照组(等体积溶剂)。采用四唑盐(MTT)比色法测定细胞活性、吖啶橙荧光染色观察细胞凋亡的形态学变化,Westernblotting分析Bcl-2、Bax和caspase-3蛋白的表达。结果:ox-LDL可明显抑制HUVEC细胞增殖,TP与ox-LDL共同加入后,细胞增殖率明显上升,与ox-LDL组相比差异显著(P<0.05)。ox-LDL可诱导细胞发生凋亡,而TP能减弱其作用。Westernblotting结果:ox-LDL下调HUVEC细胞Bcl-2表达、上调Bax和caspase-3表达,TP与ox-LDL共同加入后,Bcl-2表达升高,Bax和caspase-3表达下降。结论:茶多酚对ox-LDL诱导的HUVEC凋亡具有抑制作用,且与上调Bcl-2蛋白和下调Bax和caspase-3蛋白表达有关。     

X射线对体外培养乳鼠心肌细胞损伤的实验研究

目的 研究X射线对体外培养的心肌细胞活性及凋亡的影响。方法 体外培养新生大鼠心肌细胞,分为对照组和放射组,放射组分别用X射线10Gy、20Gy、30Gy、40Gy单剂量照射心肌细胞,采用MTT法观察X射线对乳鼠心肌细胞活性的影响;血生化自动分析仪定量测定X射线作用后心肌细胞乳酸脱氢酶(LDH)的改变;吖啶橙/碘化丙啶(AO/PI)双染色法在激光扫描共聚焦显微镜下观察心肌细胞凋亡的形态学改变;流式细胞仪定量检测心肌细胞的凋亡率。结果 ①X射线剂量在10~40Gy均能抑制心肌细胞活性并成剂量依赖性;②细胞心肌酶谱检测到LDH释放量与X射线剂量相关;③流式细胞仪发现心肌细胞凋亡率与X射线照射剂量有相关性。结论 本研究结果显示X射线对心肌细胞有毒性作用,可致心肌细胞损伤,表现为心肌细胞坏死和凋亡发生率增加。     

三种小鼠免疫细胞对辐射敏感性差异的比较

目的 对IRM-2、ICR、615三种小鼠胸腺(Th)、脾(SP)细胞照射后辐射敏感性的差异进行比较,探讨IRM-2小鼠的辐射抗性及免疫学机制。方法 用流式细胞仪检测外周血细胞分型,PA法(FITC-Annexin V和PI标记法)检测Th、SP细胞照射后凋亡率。结果 IRM-2小鼠CD4/CD8比值低于ICR、615小鼠;CD25/CD4高于615小鼠(P<0.05),低于ICR小鼠;SP细胞凋亡率0、1、4Gy低于ICR和615小鼠,差异有统计学意义(P<0.05);Th细胞凋亡率低于ICR和615小鼠,在4Gy照射组低于615小鼠(P<0.01)。结论 IRM-2小鼠的胸腺和脾细胞对辐射不敏感,辐照后Th、SP细胞凋亡率低于ICR和615小鼠。     

Involvement of inducible nitric oxide synthase in radiation-induced vascular endothelial damage

The use of radiation therapy has been linked to an increased risk of cardiovascular disease. To understand the mechanisms underlying radiation-induced vascular dysfunction, we employed two models. First, we examined the effect of X-ray irradiation on vasodilation in rabbit carotid arteries. Carotid arterial rings were irradiated with 8 or 16 Gy using in vivo and ex vivo methods. We measured the effect of acetylcholine-induced relaxation after phenylephrine-induced contraction on the rings. In irradiated carotid arteries, vasodilation was significantly attenuated by both irradiation methods. The relaxation response was completely blocked by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a potent inhibitor of soluble guanylate cyclase. Residual relaxation persisted after treatment with L-N^ω-nitroarginine (L-NA), a non-specific inhibitor of nitric oxide synthase (NOS), but disappeared following the addition of aminoguanidine (AG), a selective inhibitor of inducible NOS (iNOS). The relaxation response was also affected by tetraethylammonium, an inhibitor of endothelium-derived hyperpolarizing factor activity. In the second model, we investigated the biochemical events of nitrosative stress in human umbilical-vein endothelial cells (HUVECs). We measured iNOS and nitrotyrosine expression in HUVECs exposed to a dose of 4 Gy. The expression of iNOS and nitrotyrosine was greater in irradiated HUVECs than in untreated controls. Pretreatment with AG, L-N⁶-(1-iminoethyl) lysine hydrochloride (a selective inhibitor of iNOS), and L-NA attenuated nitrosative stress. While a selective target of radiation-induced vascular endothelial damage was not definitely determined, these results suggest that NO generated from iNOS could contribute to vasorelaxation. These studies highlight a potential role of iNOS inhibitors in ameliorating radiation-induced vascular endothelial damage.     

葡萄籽原花青素对H_20_2诱导的脐静脉内皮细胞损伤的影响

目的用葡萄籽原花青素(GSP)研究对H2O2诱导的脐静脉内皮细胞(HUVEC)损伤的保护作用及其机制。方法建立氧化损伤的细胞模型,体外培养HUVEC分为正常对照组、氧化损伤组以及高、中、低剂量(100,50,10μg/ml)GSP组;采用四甲基偶氮唑盐比色法(MTT法)检测GSP对H2O2诱导的内皮细胞氧化损伤的保护作用;逆转录聚合酶链反应(RT-PCR)检测单核细胞趋化蛋白(MCP-1)mRNA的水平;流式细胞术Annexin V/PI检测细胞凋亡以及定量检测各实验组细胞间粘附分子(ICAM-1)、血管细胞粘附分子(VCAM-1)的表达。结果内皮细胞氧化损伤后吸光度(OD)低于正常对照组;GSP预处理后OD值增加,高剂量GSP组的OD值与正常组相比无显著性差异;损伤组MCP-1 mRNA表达水平与内参照灰度值之比高于正常组;药物预处理氧化损伤后明显减弱。损伤组中细胞凋亡率显著增高、表达ICAM-1、VCAM-1的阳性细胞数均多于正常组;预处理后,凋亡细胞数以及两种粘附分子阳性细胞数明显减少,且呈剂量依赖性效应。结论葡萄籽原花青素可通过抑制内皮细胞粘附分子与细胞因子的表达而抑制炎症性损伤及其凋亡,达到保护内皮细胞的目的。     

藤黄酸通过YAP信号通路发挥对高糖诱导的内皮损伤的保护作用

目的 探讨藤黄酸在高糖诱导的内皮损伤中的保护作用及可能的作用机制。方法 人脐静脉内皮细胞（HUVEC）分5组,对照组给与低糖培养基培养,模型组和藤黄酸低剂量组、中剂量组和高剂量组均给与40mmol/L葡萄糖培养基培养,藤黄酸各给药组分别给与0.2μM、0.4μM、0.8μM藤黄酸处理,MTT检测各组细胞活力,流式细胞术检测各组凋亡,WB检测凋亡蛋白Cl-cas-3和Cl-cas-9表达,收集各组细胞上清液,检测氧化应激指标:ROS、MDA、NO以及粘附分子ICAM-1、VCAM-1水平,WB检测YAP信号通路蛋白总YAP（t-YAP）蛋白和细胞核中YAP（n-YAP）蛋白表达量。在藤黄酸处理基础上,在HUVEC细胞中过表达YAP,MTT检测细胞活力,WB检测t-YAP和n-YAP蛋白表达。结果 与对照组比较,模型组及各给药组HUVEC细胞活性明显降低、凋亡率显著增加,凋亡蛋白Cl-cas-3和Cl-cas-9表达增加,细胞中ROS、MDA水平增加,NO水平降低,ICAM-1、VCAM-1水平增加,t-YAP和n-YAP蛋白表达增加（P<0.05）,与模型组比较,藤黄酸各剂量组细胞活力显著增加、凋亡率显著降低,凋亡蛋白Cl-cas-3和Cl-cas-9表达降低,细胞中ROS、MDA水平降低,NO水平升高,ICAM-1、VCAM-1水平降低,t-YAP和n-YAP蛋白表达降低,差异均有统计学意义（P<0.05）。藤黄酸+YAP组细胞活性显著低于藤黄酸组（P<0.05）,t-YAP和n-YAP蛋白显著高于藤黄酸组（P<0.05）。结论 藤黄酸可以抑制高糖诱导的HUVEC凋亡,增强细胞活力,减轻氧化应激损伤和细胞粘附,对高糖诱导的内皮损伤发挥保护作用,机制可能与抑制YAP信号通路激活有关。     

60Co γ射线照射对体外培养的心肌细胞活性及凋亡的影响

目的研究60Co γ射线照射对体外培养的心肌细胞活性及凋亡的影响。方法体外培养新生大鼠心肌细胞,分为对照组和照射组,照射组细胞分别用60Co γ射线5Gy、10Gy、20Gy单剂量照射心肌细胞,照射后48h检测细胞培养上清中乳酸脱氢酶(LDH)浓度,流式细胞仪检测60Coγ射线照射对体外培养的心肌细胞凋亡的影响,照射后48h及120h用结晶紫试验及MTT试验检测照射后心肌细胞活性变化,结果照射组LDH浓度明显高于未照射组,且随照射剂量增加而升高。照射后48h凋亡细胞较对照组升高,凋亡细胞比例与照射剂量呈正相关。结晶紫试验及MTT试验均提示照射后48h照射组心肌细胞活细胞活性与对照组无明显差异,照射后120h照射组活细胞活性明显低于对照组,且与照射剂量相关。结论60Co γ射线单剂量照射可直接损伤心肌细胞,降低体外培养的心肌细胞活性,促进心肌细胞凋亡。     

Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53

In this study, we investigated the molecular factors determining the induction of apoptosis by radiation. Two murine tumors syngeneic to C3H/HeJ mice were used: an ovarian carcinoma OCa-I, and a hepatocarcinoma HCa-I. Both have wild type p53, but display distinctly different radiosensitivity in terms of specific growth delay (12.7 d in OCa-I and 0.3 d in HCa-I) and tumor cure dose 50% (52.6 Gy in OCa-I and > 80 Gy in HCa-I). Eight-mm tumors on the thighs of mice were irradiated with 25 Gy and tumor samples were collected at regular time intervals after irradiation. The peak levels of apoptosis were 16.1 +/- 0.6% in OCa-I and 0.2 +/- 0.0% in HCa-I at 4 h after radiation, and this time point was used for subsequent proteomics analysis. Protein spots were identified by peptide mass fingerprinting with a focus on those related to apoptosis. In OCa-I tumors, radiation increased the expression of cytochrome c oxidase and Bcl2/adenovirus E1B-interacting 2 (Nip 2) protein higher than 3-fold. However in HCa-I, these two proteins showed no significant change. The results suggest that radiosensitivity in tumors with wild type p53 is regulated by a complex mechanism. Furthermore, these proteins could be molecular targets for a novel therapeutic strategy involving the regulation of radiosensitivity.     

低剂量辐射诱导体外EL-4淋巴瘤细胞周期进程的适应性反应

目的 观察低剂量辐射诱导EL-4淋巴瘤细胞周期进程的适应性反应。方法 用X射线照射离体EL-4淋巴瘤细胞,其诱导剂量(D1)为25~200mGy(12.5mGy/min),攻击剂量(D2)为1.5Gy(287mGy/min),D1和D2间隔6h。通过流式细胞仪检测其细胞周期各时相百分数的变化。结果 当D1和D2分别为25~100mGy和1.5Gy,或分别为75mGy和0.5~2.0Gy,D1+D2各组G₀/G₁期细胞百分数不同程度低于各自D2组,而S期细胞百分数明显高于各自D2组(P<0.05、P<0.01或P<0.001)。结论 上述结果显示,EL-4淋巴瘤细胞在1.0~2.0Gy照射前6h接受25~100mGy照射,可在体外诱导其细胞周期进程的适应性反应。     

Effectiveness of carbon-ion beams for apoptosis induction in rat primary immature hippocampal neurons

The direct biological effects of radiation, particularly accelerated heavy particle ions, on neurons are not fully known. Hence, the direct effect of carbon-ion beams on immature neurons was investigated by comparing to the effect of X-rays in vitro using primary hippocampal neurons. Primary neurons were prepared from hippocampi of fetal rats at embryonic day 18 from timed pregnant Wistar rats and cultured with Banker's methods. At 7 Days In Vitro (DIV), the cells were irradiated with 140 kV X-ray and 18.3 MeV/amu carbon-ion beams (LET = 108 keV/μm). The cells were fixed with 4% paraformaldehyde at 12 hours after irradiation. Then, the cells were treated with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and DAPI staining for measuring the percentage of apoptosis (apoptotic index: AI). AI in sham-irradiated hippocampal neurons was 18%. The value of AI (AIs) of the cells irradiated with X-rays at 10 or 30 Gy were 15% or 23%, respectively. AI in cells irradiated with carbon-ion beams at 1 Gy, 3 Gy, 5 Gy and 10 Gy were 22%, 23%, 24% and 33%, respectively. AI was significantly increased by carbon-ion beams at 10 Gy (p < 0.001). The apoptosis of hippocampal neurons increased in a dose-dependent manner following both X-ray and carbon-ion beams irradiation. Carbon-ion beams were about 10-fold more effective than X-rays for apoptosis induction in immature hippocampal neurons.     

低剂量X射线对脐静脉内皮细胞分泌vWF的影响

目的 探讨低剂量X射线（0.1 Gy）照射对脐静脉内皮细胞分泌vWF的影响。方法 采用医用直线加速器对脐静脉内皮细胞进行0、0.1 Gy（剂量率为200 cGy/min）的X射线照射,然后采用MTT法、台盼蓝染色和细胞凋亡实验检测细胞增殖、细胞活力及细胞凋亡。此外,采用ELISA和Westernblot方法检测受X射线照射后的细胞培养液中vWF的表达。结果 以0.1 Gy的低剂量X射线照射脐静脉内皮细胞后,细胞增殖、细胞活力以及细胞凋亡的结果与对照组相比无统计学差异,但照射后的脐静脉内皮细胞培养基中vWF水平明显升高。结论 低剂量（0.1 Gy）的X射线剂量照射不会导致脐静脉内皮细胞增殖、凋亡或细胞活性的显著改变,但是促使其分泌vWF的量增多。     

E-Selectin expression in human endothelial cells exposed to PM10: the role of endotoxin and insoluble fraction

Exposure to PM10 is associated with cardiovascular effects. We evaluated the effects of PM10 on E-Selectin expression and monocytic cell adhesion in human umbilical vein endothelial cells (HUVECs). HUVEC were exposed to PM10 (5-40 microg/cm2) for 6 h, following which surface E-Selectin expression was detected by fluorescence microscopy and flow cytometry. The effects of total particles, particles treated with polymixin-B to block the effects of endotoxin, and both soluble and insoluble fractions of particles, were assessed. Incubation with PM10 lead to a concentration-related increase of E-Selectin expression (>seven-fold increase at 40 microg/cm2). Particles pre-treated with polymixin-B inhibited E-Selectin expression to a level slightly higher than untreated particles. An increase in fluorescence was also observed with the insoluble fraction, while the soluble fraction had no significant effect. HUVEC exposed to PM10 were also evaluated for adhesivity of monocytic cells (U937). PM10 strongly increased the adhesion of U937 cells to HUVEC. In conclusion, PM10 induces endothelial cell activation, evidenced by enhanced E-Selectin expression. This activation is manifested functionally as an increase in monocytic cell adhesion. Insoluble components as well as endotoxins appear to be responsible for this activity.     

枸杞多糖对慢性辐射小鼠细胞凋亡及bc1-2基因表达的影响

目的:探讨枸杞多糖(LBP)对辐射小鼠细胞凋亡及凋亡相关基因bcl-2表达的影响。方法:以水提取-乙醇沉淀法制备枸杞多糖,并制成0.8%的饲料,给予受试小鼠(枸杞多糖组)。正常对照组、辐射对照组给予普通饲料。除正常对照组外,另两组均用60Coγ射线对动物进行全身性照射,每天照射1次,每天照射剂量为0.084Gy,每周照射5d,连续照射6w,照射总剂量为2.52Gy。检测骨髓微核率、睾丸精母细胞染色体畸变、精子畸形率、肝细胞caspase-3mRNA表达水平、细胞凋亡及凋亡相关基因bc1-2表达等指标。结果:LBP可使辐射引起的微核率、染色体畸变、及精子畸形率显著降低,骨髓细胞增殖活性提高,凋亡率降低,使辐射小鼠bc1-2基因表达提高、caspase-3mRNA表达水平降低。结论:枸杞多糖的抗辐射作用与其调控细胞bc1-2基因表达,影响细胞凋亡有关。     

Gene expression and cell cycle arrest in a rat keratinocyte line exposed to 56Fe ions

The purpose of the present work was to examine gene expression patterns in a rat keratinocyte line exposed to a (56)Fe ion beam. The cells were exposed to 1.01 geV/nucleon (56)Fe ions generated by the NASA Space Radiation Laboratory facility. Data from Affymetrix rat microarrays (RAT 230_2) were processed by BRB ArrayTools 3.3.0 software, and the Gene Ontogeny (GO) database was utilized to categorize significantly responding genes. Cell cycle distribution was analyzed by flow cytometry, and cell survival was based on the colony survival assay. At 24 h after 3.0 Gy of (56)Fe ion radiation, 69 known genes were significantly (p 相似文献   

同型半胱氨酸诱导内皮细胞凋亡及叶酸的拮抗机制———Caspase3及其抑制蛋白c-IAP1和c-IAP2的作用

目的　本研究探讨同型半胱氨酸 (Hcy)致内皮细胞凋亡的途径以及叶酸拮抗Hcy的机制。方法　Hcy、叶酸或二者联合处理人脐静脉内皮细胞 (HUVEC) 2 4小时后 ,用AnnxinV染色加流式细胞术及基因组DNA电泳检测DNAladder了解细胞凋亡状态 ;RT PCR和蛋白质印迹技术检测caspase3、c IAP1和c IAP2的mRNA和蛋白质水平。结果　 0 3mmol L和 3 0mmol L的Hcy均导致HUVEC凋亡 ,Hcy浓度高时凋亡细胞数较高 ,并伴有caspase3表达和活化增强 ,以及c IAP2的mRNA和蛋白质水平降低 ;叶酸可上调c IAP2的表达。结论　Hcy诱导HUVEC凋亡 ,此种作用可能涉及caspase3相关途径。叶酸可促进c IAP 2表达 ,从而部分拮抗Hcy的作用。     

重度妊娠高血压综合征患者血清诱导的脐血管内皮细胞凋亡失衡与肿瘤坏死因子的关系

目的:探讨重度妊娠高血压综合征(简称妊高征)患者血清对体外培养的脐血管内皮细胞(HUVEC)凋亡和对抑／促凋亡基因Bcl-2／Bax表达的影响以及与肿瘤坏死因子α(TNFα)的关系。方法:体外培养HIJVEC,加入重度妊高征患者血清和TNFα作为处理因素,免疫细胞化学检测Bcl-2／Bax蛋白表达;流式细胞仪做凋亡细胞记数;扫描电镜观察细胞变化。结果:轻重度妊高征患者血清处理后的HUVEC Bcl-2／Bax表达失衡,凋亡细胞数增加,扫描电镜可见经TNFα处理后的内皮细胞变圆,微绒毛消失,密度增高,可见凋亡小体。结论:TNFα可诱导体外培养的脐血管内皮细胞凋亡,并可引起凋亡相关基因Bcl-2／Bax表达失衡,可能是引起妊高征血管内皮细胞损伤的原因之一。     

Radiation-induced ICAM-1 expression via TGF-β1 pathway on human umbilical vein endothelial cells; comparison between X-ray and carbon-ion beam irradiation

Adhesion of inflammatory cells to endothelial cells is considered to be involved in the process of radiation-induced damage and fibrosis. Intercellular adhesion molecule-1 (ICAM-1) and transforming growth factor-beta1 (TGF-β1) are thought to play important roles in this process. In this study, radiation-induced ICAM-1 expression on endothelial cells was investigated with the use of an inhibitor of TGF-β1 receptor kinase (SB431542) and the effects of X-ray and carbon-ion beam were compared. Cell cultures of human umbilical vein endothelial cells (HUVE cells) were incubated with TGF-β1 and irradiated with 140 KV X-ray. Next, HUVE cells were irradiated with X-ray and 220 MeV carbon-ion beam with or without SB431542. Immunofluorescence analysis was used to quantify ICAM-1 expression. The expression of ICAM-1 on HUVE cells was significantly increased by the stimulation with TGF-β1. Expression of ICAM-1 was increased by X-ray and carbon-ion beam irradiation and decreased significantly with SB431542 after both irradiations. The expression of ICAM-1 by 2 Gy of carbon-ion beam irradiation was 6.7 fold higher than that of non-irradiated cells, while 5 Gy of X-ray irradiation increased the expression of ICAM-1 by 2.5 fold. According to ICAM-1 expression, the effect of carbon-ion beam irradiation was about 2.2, 4.4 and 5.0 times greater than that of the same doses of X-ray irradiation (1, 2 and 5 Gy, respectively). The present results suggested that radiation-induced ICAM-1 expression on HUVE cells was, at least partially, regulated by TGF-β1. Carbon-ion beam induced significantly higher ICAM-1 expression than X-ray.