19 MeV质子辐照小鼠损伤效应研究

目的探讨质子辐照对小鼠死亡率及主要器官损伤病理学改变的影响，为保证载人航天航天员的健康和生命安全提供参考。方法ICR小鼠，体重20～22g，随机分为对照组和辐照剂量分别为4、8、16和32Gy4个辐照组，用氯胺酮（0．05ml／只）麻醉，将小鼠用透明胶粘住鼠尾和后肢，两只并排，将背部固定于辐射范围内（7．5cm^2）。采用中国原子能科学研究院的北京HI-13串列加速器加速的19MeV质子，轰击1．3mg／cm^2的Au靶，在大气环境下对小鼠进行均匀辐照。辐照后常规测定各组外周血网织红细胞的变化，同时观察小鼠死亡率。辐照第14天，动物再次称重后活杀，行解剖学和光镜检查。结果发现32Gy质子照射组小鼠（n=4）在14d内全部死亡，16Gy质子照射组小鼠14d内死亡1／5，4和8Gy组小鼠30d内全部存活：在照射小鼠背部7d后出现损伤带，表现为随着剂量的增加，损伤带脱毛、皮肤灼伤程度加重。照射后小鼠外周血网织红细胞明显增多，脾小体明显缩小，骨髓出血、水肿、坏死，造血细胞减少，肺组织出血、水肿，细胞数量减少，皮肤变性、水肿，皮肤表皮和真皮纤维组织增生，表皮局部坏死脱落，毛囊和皮脂腺减少，睾丸曲细精管生精上皮细胞部分变性、坏死。结论本研究证实质子辐射对小鼠血液网织红细胞动态变化和死亡率及主要器官损伤病理学改变的影响明显，迫切需要深入研究。     

高功率毫米波急性持续辐照对小鼠皮肤损伤的影响

目的 研究高功率毫米波(HPMMW)对急性持续辐照致死小鼠皮肤的损伤效应.方法 使用34.1 GHz毫米波源,分别连通4种角锥喇叭天线垂直辐照小鼠背侧,输出平均功率分别为5、10、12W,辐照距离分别为角锥喇叭天线垂直下方10、20mm,持续辐照直至小鼠死亡.取辐照区域皮肤并立即置于4%甲醛溶液中固定.制备石蜡切片,经HE、天狼猩红染色后进行图像采集,使用图像分析软件(ImageProPlus)定量分析皮肤各层结构的病理变化.结果 受辐照小鼠均出现不同程度皮肤损伤,其中喇叭天线HD-320HA24.12辐照组小鼠存活时间较长,皮肤表现为慢性损伤,真皮胶原纤维密度降低、消失,皮下脂肪层变薄甚至消失,肌细胞排列稀疏等.喇叭天线HD-320HA23.16组小鼠存活时间最短,皮肤表现为严重急性损伤,真皮层胶原纤维密度增加甚至无间隙,肌细胞排列稀疏等.喇叭天线HD-320HA9.49和HD-320HA9.92的损伤类型与急性损伤类似.结论 HPMMW急性持续辐照可导致小鼠皮肤损伤,其中高强度辐照可导致皮肤急性损伤,而低强度辐照可导致皮肤慢性损伤,所造成的皮肤损伤可深达小鼠皮下深层组织,各组肌肉层的损伤程度基本相同,真皮层的损伤形式与HPMMW的作用强度和时间有关.真皮层纤维组织及皮下肌细胞的密度和分布形式可作为评价皮肤损伤程度的指标,为深入研究毫米波对皮肤的损伤规律和机制提供依据,并为电磁辐照生物效应的定量化研究提供参考.     

双光子成像技术在大鼠放射性皮肤损伤修复评估中的应用

目的 采用双光子激发荧光（TPEF）成像技术,无创、活体评估X射线引起大鼠皮肤放射性损伤发展和修复过程。方法 24只SD大鼠采用随机数表法分为4组,健康对照组、25 Gy组、35 Gy组和45 Gy组,每组6只。照射后不同时间评估皮肤损伤程度,通过TPEF成像技术在体检测表皮细胞尼克酰胺腺嘌呤二核苷酸（磷酸）[NAD（P）H]和真皮胶原纤维荧光信号的病理改变。结果 第10天,各辐射组大鼠出现红斑和脱皮;第15~20天,随着辐射剂量地增加,辐射组出现递进性的渗出、水肿和溃疡;第25天,25 Gy组开始修复,其他组仍有渗出和溃疡。第10天,25、35和45 Gy组表皮细胞NAD（P）H荧光信号减少,乳头层和网状层荧光信号值减少,与健康对照组比较,差异有统计学意义（t=24.145、28.303、26.989、6.654、7.510、7.997,P<0.05）;第30天,25 Gy组表皮细胞NAD（P）H和真皮胶原纤维开始修复,颗粒层、棘层和基底层细胞出现荧光信号,35、45 Gy组未出现NAD（P）H荧光信号;25 Gy组乳头层和网状层荧光信号均逐渐增高,但仍低于健康对照组（t=115.133、17.431,P<0.05）,而45 Gy组未出现荧光信号。结论 TPEF技术可以无创、活体检测X射线照射后表皮细胞和真皮胶原纤维信号损伤和修复的病理变化。     

3D打印皮肤成体干细胞来源类器官人工皮肤修复小鼠皮肤缺损

目的构建3D打印皮肤成体干细胞来源类器官人工皮肤并探讨其修复小鼠皮肤缺损的效果。方法将人皮肤角质形成细胞、成纤维细胞、血管内皮细胞以2∶1∶1制备细胞混合悬液, 在超低吸附培养板中培养, 倒置相差显微镜观察细胞球的形态变化。培养7 d后收集细胞球, 进行免疫荧光染色, 检测其真皮、表皮及血管标志物的表达情况及结构分布情况。采用3D打印技术打印类器官人工皮肤, 观察打印出的人工皮肤的形态。将10只免疫缺陷balb/c雌性小鼠按随机数字表法分为水凝胶组和类器官组, 每组5只。所有小鼠建立直径1 cm的全层皮肤缺损模型, 水凝胶组创面覆盖水凝胶敷料, 类器官组创面覆盖相同大小类器官人工皮肤。建模后0、4、8、12及16 d观察两组创面愈合大体情况及创面愈合率。建模后16 d时创面皮肤取材, HE染色观察创面表皮角化情况及表皮真皮连接情况, Masson染色观察创面胶原纤维的疏松致密程度及真皮层纤维厚度。结果 (1)角质形成细胞、成纤维细胞、血管内皮细胞的细胞混合悬液在超低吸附培养板中可自聚集形成细胞球;倒置显微镜观察显示, 随着培养时间延长, 细胞球体积逐渐增大。(2)细胞球免疫荧光染色结果...     

阿的平对微波辐射小鼠海马损伤的保护作用

目的探讨预先给予阿的平（quinacrine）对微波辐射致小鼠脑损伤的保护作用。方法小鼠随机分为4组,即正常组、辐射对照组、阿的平低剂量组（12.6 mg/kg）、阿的平高剂量组（50.4 mg/kg）。接受辐射动物于照射后即刻（0 d）,1,2,7 d后完成检测,正常组动物在辐射实验后7 d后完成检测。微波辐照后,于不同时间点提取小鼠的脑组织蛋白,检测脑组织中HSP70蛋白表达变化。结果脑组织蛋白表达检测显示,微波辐射后1 d,辐射对照组小鼠脑中HSP70蛋白的表达开始升高,直至7 d。阿的平两个剂量组0,1,7 d给药组与辐射对照组相比明显上调,高剂量组尤甚。辐射对照组小鼠大脑海马的病理切片显示细胞水肿、血管扩张肿胀、间质充血等损伤,并出现海马沟回组织松散、细胞核皱缩、细胞水肿、空泡现象。预先灌胃给予小鼠阿的平后,小鼠脑组织的病理损伤有所减轻,状况有所改善。结论阿的平的这些保护机制可能与其上调HSP70蛋白表达发挥抗炎和抗凋亡作用,降低微波辐照引起的组织、细胞炎症反应和凋亡、坏死有关。     

532nm连续激光照射下鸡冠组织热效应的动物实验研究

目的观察532 nm连续激光照射下鸡冠组织的温度变化,为光动力疗法（photodynamic therapy,PDT）治疗鲜红斑痣（port wine stain,PWS）中激光光剂量的安全性提供实验依据。方法将雄性3月龄白羽鸡30只,按功率密度100、150、200、250和300 mW/cm^2随机分为5组,每组6只。采用波长532 nm全固态激光器照射2 cm×2 cm鸡冠组织,照射时间20 min。照光同时应用热红外成像温度监测仪对照射区域的鸡冠组织进行连续温度成像监控。分别于照射后即刻、1和3 d对鸡冠组织进行大体观察,3d后进行病理学检查,观察血管和表皮损伤情况。结果在照光过程中,各组温度变化都呈现单边上升、达到平台的变化规律：功率密度为100、150、200、250和300 mW/cm^2组,温度最高值分别为45.1℃、49.9℃、51.6℃、51.8℃和53.7℃,达最高温度时间分别为20、16、7、6和6 min。鸡冠大体损伤和病理损伤随温度升高而加重,200 mW/cm^2以上功率密度导致鸡冠表皮和真皮凝固性坏死。结论在532 nm连续激光照射下,鸡冠组织的温升程度和损伤程度随着功率密度的增加逐渐增高,150 mW/cm^2以下功率密度较为安全。     

白藜芦醇通过Akt/mTOR通路上调自噬改善辐射诱导小肠损伤

目的探讨白藜芦醇是否能够通过调节Akt/mTOR通路改善辐射诱导小肠损伤并研究其机制。方法将24只C57BL/6小鼠随机分为对照组、照射组和照射给药组(每组8只)。照射组和照射给药组小鼠接受9.0 Gy剂量的6MV-X射线全身照射,照射给药组小鼠在照射前3 d至照射后3 d每日腹腔注射白藜芦醇(50 mg·kg~(-1)·d~(-1)),对照组、单纯照射组予等量生理盐水。照射后3.5 d获取小肠组织并制作石蜡块后切片,采用HE染色及免疫组织化学染色行组织学分析;行Western blot试验检测p-Akt/Akt、p-S6RP/S6RP、LC3-Ⅱ、Beclin-1表达。采用ANOVA方差分析进行3组间比较。结果照射给药组小鼠小肠绒毛长度、小肠横断面隐窝数、单个小肠隐窝细胞总数、隐窝细胞Ki67阳性率均高于照射组(均P0.05);照射给药组较照射组小肠组织p-Akt/Akt、p-S6RP/S6RP蛋白表达下降(均P0.001),LC3-Ⅱ、Beclin-1蛋白表达升高(均P0.001)。结论白藜芦醇可能通过抑制Akt/mTOR通路促进受辐射小鼠小肠隐窝细胞自噬从而改善辐射诱导小肠损伤。     

电磁脉冲辐射对小鼠睾丸结构的影响

目的 :探讨不同场强的电磁脉冲辐射对睾丸结构的影响。方法 :二级昆明雄性小鼠 114只 ,随机分为辐射组和对照组。辐射组小鼠分别接受 8× 10 3 ,2× 10 4,6× 10 4V/m电磁脉冲 5次重复全身照射 ,于照射后 6h ,1d ,3d ,7d ,14d和 2 8d观察睾丸和附睾病理学改变。结果 :3种场强的电磁脉冲辐射均未引起小鼠肛温和阴囊皮肤温度的明显升高 ,但睾丸却发生显著的各级生精细胞水肿、坏死和脱落 ,曲细精管内成熟精子稀少和缺失 ;最敏感的靶细胞是精原细胞和精子细胞 ;周边部曲细精管病变最明显 ;病变的严重程度与场强的大小呈正相关。结论 :8× 10 3 ～ 6× 10 4V/m电磁脉冲 5次重复全身照射小鼠 ,可引起小鼠睾丸严重的非热效应性生精细胞结构损伤。     

西咪替丁对急性照射小鼠存活率及造血系统改变的影响

目的 观察西咪替丁对急性照射小鼠存活率及造血系统改变的影响.方法 采用137Cs γ射线全身照射小鼠,两次实验的照射剂量分别为6.0Gy和8.0Gy,剂量率均为1.01Gy/min.每次实验取健康雄性C57BL/6小鼠60只,按体重随机分为空白对照组?模型对照组?阳性药组(523)及33.3?100?300mg/kg西咪替丁组,每组10只.西咪替丁各剂量组于照射前6d灌胃给药,每天1次,照射后5h给药1次;阳性药组于照射前1d灌胃给药1次,照射后5h给药1次.检测8.0Gy照射后30d小鼠存活率,以及6.0Gy照射后30d小鼠外周血象?骨髓DNA含量和骨髓嗜多染红细胞微核率.结果8.0Gy照射后,模型对照组小鼠于第21天全部死亡,西咪替丁低?中?高剂量组30d存活率分别为50%?20%和30%;6.0Gy照射后第30天,与空白对照组比较,各照射组小鼠外周血白细胞明显降低(P<0.01),骨髓嗜多染红细胞微核率明显升高(P<0.05),骨髓DNA含量明显降低(P<0.05);与模型对照组比较,西咪替丁高剂量组外周血白细胞明显升高(P<0.01),西咪替丁各剂量组骨髓DNA含量明显升高(P<0.01,P<0.05),而骨髓嗜多染红细胞微核率明显降低(P<0.01,P<0.05)并趋于正常.结论 西咪替丁能提高急性照射小鼠30d存活率,且对其造血系统有较好的保护作用.     

超高剂量率照射与常规照射后胶质瘤小鼠血浆代谢物时序性特征对比分析

目的探究超高剂量率照射(FLASH-RT)和常规照射(CONV-RT)对胶质瘤小鼠血浆代谢物的影响。方法胶质瘤模型雄性C57BL/6J小鼠21只, 按随机数表法分成健康对照组(3只)、CONV-RT组(9只)和FLASH-RT组(9只)。CONV-RT组以0.4 Gy/s的剂量率对小鼠头部进行单次24 Gy照射, FLASH-RT组以60 Gy/s的剂量率对小鼠头部进行单次24 Gy照射, 健康对照组以相同条件给予0 Gy假照射。两照射组照射后1、3、7 d分别收集小鼠眼内眦静脉血并分离血浆。健康对照组于假照射后7 d收集小鼠眼内眦静脉血并分离血浆。采取基于液相色谱质谱串联平台的非靶向代谢组学方法检测胶质瘤小鼠血浆代谢物的变化。结果胶质瘤小鼠受不同方式照射后, 血浆中代谢物均发生显著变化。FLASH-RT组和CONV-RT组3个时间点分别与健康对照组相比筛选出12和5种差异代谢物, 照后1 d血浆代谢物差异最大, 照后3和7 d血浆代谢物差异减小。FLASH-RT组筛选出的花生四烯酸与异戊酸也存在于CONV-RT组中, 其余10种差异代谢物仅存在FLASH-RT组, 主要涉及能量代谢和...     

Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-dimethybenz[alpha]anthracene

PURPOSE: Although radiofrequency (RF) radiation is not considered mutagenic, it has been suggested as a promoter of tumorigenesis. To study if RF radiation has a tumor promoting effect, we exposed mice with skin tumorigenesis initiated by 7,12-dimethybenz[a]anthracene (DMBA) to RF radiation. MATERIALS AND METHODS: Eighty male ICR mice were subjected to a single DMBA application (100 microg/100 microl acetone/mouse) on shaved dorsal skin at the age of 7 weeks. After one week, the mice were randomized into four equal groups of 20 mice each: i.e., sham-, 849 MHz-, 1,763 MHz-exposed, and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated groups. The RF exposure was conducted at a whole body average specific absorption rate (SAR) of 0.4 W/Kg, for 2 cycles of 45 min exposure with a 15 min interval each day, 5 days a week for 19 weeks. The TPA-treated group served as a positive control for skin tumorigenesis and were administered TPA (4 microg/100 microl acetone/mouse) twice weekly without RF exposure. RESULTS: All mice were examined weekly at a macroscopic level. No skin tumors were observed in any groups except in the TPA-treated positive control group. TPA is known tumor promoter in DMBA-induced skin carcinogenesis and tumor incidence in the TPA treated group was 95%. At week 20 after DMBA initiation, skin tissues were analyzed immunohistochemically using anti-proliferating cell nuclear antigen (PCNA) antibody. No differences were observed by pathological examination or by PCNA staining between the sham- and the RF-exposed groups. The expression of cyclin D1 and c-fos were detected only in the tumorous skin tissues of the TPA-treated group. CONCLUSION: No evidence was found that RF radiation serves as a tumor promoter for skin tumors. Our data suggests that 849 MHz and 1,763 MHz RF radiations, similar to those emitted from mobile phones, do not have any promoting effect on skin tumor development in DMBA-initiated mice.     

Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-dimethybenz[α]anthracene

Purpose: Although radiofrequency (RF) radiation is not considered mutagenic, it has been suggested as a promoter of tumorigenesis. To study if RF radiation has a tumor promoting effect, we exposed mice with skin tumorigenesis initiated by 7,12-dimethybenz[α]anthracene (DMBA) to RF radiation.

Materials and methods: Eighty male ICR mice were subjected to a single DMBA application (100 μg/100 μl acetone/mouse) on shaved dorsal skin at the age of 7 weeks. After one week, the mice were randomized into four equal groups of 20 mice each: i.e., sham-, 849 MHz-, 1,763 MHz-exposed, and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated groups. The RF exposure was conducted at a whole body average specific absorption rate (SAR) of 0.4 W/Kg, for 2 cycles of 45 min exposure with a 15 min interval each day, 5 days a week for 19 weeks. The TPA-treated group served as a positive control for skin tumorigenesis and were administered TPA (4 μg/100 μl acetone/mouse) twice weekly without RF exposure.

Results: All mice were examined weekly at a macroscopic level. No skin tumors were observed in any groups except in the TPA-treated positive control group. TPA is known tumor promoter in DMBA-induced skin carcinogenesis and tumor incidence in the TPA treated group was 95%. At week 20 after DMBA initiation, skin tissues were analyzed immunohistochemically using anti-proliferating cell nuclear antigen (PCNA) antibody. No differences were observed by pathological examination or by PCNA staining between the sham- and the RF-exposed groups. The expression of cyclin D1 and c-fos were detected only in the tumorous skin tissues of the TPA-treated group.

Conclusion: No evidence was found that RF radiation serves as a tumor promoter for skin tumors. Our data suggests that 849 MHz and 1,763 MHz RF radiations, similar to those emitted from mobile phones, do not have any promoting effect on skin tumor development in DMBA-initiated mice.     

Effect of radiophsophorus on hematology of mice during postnatal development.

Swiss albino mice at different stages of their postnatal development (one day, one week, two weeks, three weeks, four weeks age groups) were injected intraperitoneally with radioactive phosphorus (P-32) at the dose of 1.0 muCi/g body weight and studied for their hematological response at weekly intervals up to six weeks of age when they attain sexual maturity. In all the treated groups in both males and females, the radiation injury was evident after injection of radioactive phosphorus. Animals showed reduction in blood cell number and fall in hemoglobin and hematocrit levels after injection. Reparation was also evident in the animals after some lapse of time following P-32 administration. Morphological changes in different white blood cells were not observed. No radiation sickness symptoms were observed in any of the treated groups during the study. There was no radiation mortality. The radiation damage to blood forming organs was moderate. It was observed that the females showed a greater hematological damage than the males.     

Time course of loss of residual radiation damage in murine skin assessed by retreatment

The amount of radiation damage remaining in mouse foot skin has been assessed by retreatment from 10 days to 6 months after a range of first doses. The acute skin reaction was used as the endpoint. Mice hind feet were first irradiated with a range of single doses (15-37.5 Gy) covering zero to near full effect. Feet were retreated with a full range of single doses together with groups of non-previously treated age-matched control mice. No age-related changes in radiation sensitivity were observed. Dose-response curves were constructed for all retreatment times for each priming dose, and isoeffect doses were calculated for both peak and average skin reactions. If 2-6 months were allowed to elapse before retreatment, the skin could be reirradiated as if it were previously untreated. However, if only 1 month was allowed to pass before retreatment, damage was 'remembered' after all first doses. The amount of damage 'remembered' in terms of dose was 11 Gy after a first dose of 37.5 Gy, and was less after the lower first doses.     

湿润烧伤膏联合龙血竭防治乳腺癌改良根治术后放射性皮肤损伤疗效观察

目的对比分析湿润烧伤膏联合龙血竭防治乳腺癌改良根治术后放射性皮肤损伤的临床疗效。方法将2015年8月至2018年8月临沂市第三人民医院收治的120例乳腺癌改良根治术后行放射治疗的患者按照治疗方法分为观察组(60例)、对照1组(30例)与对照2组(30例),观察组患者放射治疗后照射区域皮肤均匀涂抹湿润烧伤膏,出现Ⅱ~Ⅳ级放射性皮肤损伤时加用龙血竭粉末外敷;对照1组患者放射治疗后照射区域皮肤均匀涂抹湿润烧伤膏,出现Ⅱ~Ⅳ级放射性皮肤损伤时继续应用湿润烧伤膏换药治疗;对照2组患者放射治疗后照射区域皮肤不采取防护措施,出现Ⅱ~Ⅳ级放射性皮肤损伤时予以碘伏常规换药治疗。对比观察3组患者放射性皮肤损伤发生情况、放射治疗中断情况及临床疗效结果放射治疗20 Gy、40 Gy及结束后,3组患者皮肤损伤发生情况对比,χ~2=59.417、94.876、29.072,P均=0.000,差异具有统计学意义,且对照2组患者皮肤损伤发生情况较观察组及对照1组严重(放射治疗20Gy后:χ~2=41.918、23.721,P均=0.000;放射治疗40 Gy后:χ~2=74.118、47.368,P均=0.000;放射治疗结束后:χ~2=61.606、30.610,P均=0.000),而观察组与对照1组患者皮肤损伤发生情况无明显差异(P均>0.05)。放射治疗过程中,对照2组中有7例患者因放射性皮肤损伤中断治疗,明显高于观察组与对照1组均无患者中断治疗(χ~2=15.181、7.925,P=0.000、0.005)。放射治疗结束后2周,观察组患者的临床疗效明显优于对照1组及对照2组(χ~2=6.923、24.761,P=0.009、0.000),而对照1组患者的临床疗效明显优于对照2组(χ~2=8.324,P=0.016)。结论湿润烧伤膏联合龙血竭可有效防治乳腺癌改良根治术后放射性皮肤损伤,促进放射性皮肤损伤创面愈合,避免放射治疗中断,且操作简便,值得临床推广应用。     

The effect of evening primrose oil on the radiation response and blood flow of mouse normal and tumour tissue

PURPOSE: To investigate the effect of the oral administration of evening primrose oil on the radiation response and the blood flow of normal tissue and a tumour in BALB/c mice. METHODS AND MATERIALS: Aliquots of evening primrose oil were fed to BALB/c mice daily and the radiation response of the skin was assessed by the determination of ED50 values for the incidence of moist desquamation, using probit analysis. Tumour radiosensitivity was investigated by determining the growth delay caused by irradiation of a transplantable rhabdomyosarcoma. The 86RbCl uptake technique was used to determine the blood flow in normal foot and tumour tissue. The fatty-acid content of red blood cells, plasma and tumour tissue was measured using gas chromatography. RESULTS: Daily evening primrose oil dietary supplementation reduced the sensitivity of skin to radiation-induced moist desquamation and prevented the radiation-associated increase in blood flow that was observed in this tissue. No modification of tumour blood flow or of tumour sensitivity to radiation resulted from evening primrose oil supplementation of mice. Evening primrose oil supplementation resulted in changes in plasma levels of linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA). These changes were contingent on whether the mice had been irradiated or not. In red blood cells evening primrose oil supplementation increased the GLA level of unirradiated mice and the LA level at 20 days after irradiation. There were no changes in tumour fatty-acid levels as a result of evening primrose oil treatment. CONCLUSIONS: Daily evening primrose oil supplementation reduced the sensitivity of skin to radiation-induced moist desquamation but did not alter tumour sensitivity to radiation.     

甘草黄酮对小鼠光老化皮肤中caspase-3、caspase-12表达的影响

目的:研究皮肤外用甘草黄酮对紫外线照射引起的小鼠光老化皮肤的影响。方法:BALB/C小鼠50只随机分成5组:模型组(A)、基质组(B)、甘草黄酮组(C)、薇诺娜组(D)、正常对照组(E),模拟UVB长期照射,造成皮肤光老化小鼠模型。B、C、D组照射同时分别外用基质乳膏、甘草黄酮乳膏、薇诺娜防晒霜(SPF30,PA+++)。组织切片HE染色观察皮肤结构改变;以ELISA法测定皮肤组织caspasse-3、caspase-12含量。结果:A、B组小鼠皮肤组织caspasse-3、caspase-12含量明显增加,病理切片呈现明显光老化状态;C、D组cspasse-3、caspase-12含量与E组差异无统计学意义(P>0.05)。结论:甘草黄酮乳膏对紫外线照射引起的小鼠皮肤光老化具有保护作用,其机制可能为甘草黄酮通过抑制caspase-12活化,进而阻断caspase-3的激活,抑制细胞的凋亡。     

EGFR、Bax、Rb在高能电子线大鼠皮肤辐射损伤模型中的表达和意义

目的：探讨EGFR、Bax、Rb在高能电子线大鼠皮肤辐射损伤中的作用及机理,为临床治疗提供线索。方法：运用免疫化技术SP法检测EGFR、Bax、Rb在40例高能电子线大鼠皮肤辐射损伤模型中的表达,分析它们与照射剂量之间的关系。结果：（1）EGFR在40例照射的大鼠中,5、15、30、45Gy组阳性表达率分别为20％、40％、70％、100％;各照射剂组间有显著相关性（P＜0．05）。（2）Bax在40例照射的大鼠中,5、15、30、45Gy组阳性表达率分别为30％、30％、70％、70％;各照射剂量组同Bax蛋白阳性表达无相关性,但有趋势性（P＜0．05）。（3）Rb在40例照射的大鼠中5、15、30、45Gy组阳性表达率分别为30％、20％、40％、30％;各照射剂量组间Rb阳性表达无线性趋势性（P＞0．05）。（4）本实验对40例各照射剂量组实验对象研究发现Bax^ /Rb^ 共有9例,EGFR^ /Rb^ /Bax^ 共有5例,均无共同阳性趋势。结论：实验表明电离辐射能增加大鼠皮肤组织中EGFR、Bax、Rb蛋白的表达;EGFR、Bax蛋白的表达可能与照射剂量有关;EGFR能促进细胞的增殖与Bax,Rb蛋白促细胞凋亡共同作用下,参与3放射性皮肤损伤的形成。     

褐藻糖胶对60Co-γ 射线照射小鼠造血系统的辐射防护作用研究简

目的观察褐藻糖胶对^60Co-γ射线照射小鼠体内造血系统的辐射防护作用。方法以BALB／c小鼠进行体内照射,一次性全身照射前腹腔注射给予褐藻糖胶3d,测定脾指数、脾脏内部结构以及内源性脾结节数（7．5Gy）、骨髓有核细胞计数（6．0Gy）、外周血象（5．5Gy）。结果小鼠体内造血系统实验显示7．5Gy^60Co-γ照射后,各给药照射组的脾指数及内源性脾结节数明显较对照组增多,中剂量照射组的脾脏大小以及脾脏内部组织结构均比对照组有显著的差别;6．0Gy^60Co-γ照射后,小鼠骨髓有核细胞数较正常对照组相比差异非常显著（P〈0．01）,各给药照射组与照射对照组比较,均高于照射对照组（P〈0．05或P〈0．01）：5．5Gy^60Co-γ照射后30d,小鼠外周血象测定中各给药照射组白细胞数明显高于对照组（P〈0．01）,而外周血红细胞、血红蛋白和血小板无明显影响。结论褐藻糖胶对^60Co-γ射线照射引起的小鼠造血系统损伤有保护作用。     

全脑常规照射开放血脑屏障动物模型的建立

目的 建立全脑常规照射开放血脑屏障（blood—brain barrier，BBB）的鼠动物模型。方法 100只SD大鼠随机分为5组，依次为假照射组、10、20、30和40Gy组，每组20只，^60Coγ射线全脑常规照射，2Gy，次，5次，周，每日观察大鼠饮食、自主活动、并记录照射区皮肤与毛发、体重及神经系统症状变化，照射后16h每组随机选取4例用镧示踪电镜化学技术观察大鼠BBB超微结构的变化。结果实验大鼠均未出现可评价的异常神经行为及体征；各组的饮食、自主活动、皮肤与毛发无可评价的异常改变；体重增加无统计学意义（P〉0．05）。透射电镜观察显示照射后随照射剂量的增加出现BBB功能的改变，且与照射剂量呈正相关。结论该模型能较好地模拟临床放射治疗过程，易于操作，成功率高，是全脑常规照射后从病理生理学及分子生物学等方面研究BBB功能变化规律的良好模型。