照射和电击对大鼠性激素,肝功能和脂质过氧化物的影响

本文观察了长期低剂量ν射线照射和照射加电击对中年大鼠血浆性激素水平、肝微粒体细胞色素P-450浓度和混合功能氧化酶(MFO)活力的影响。照射组与照射加电击组雄性大鼠血浆睾酮水平明显降低(分别为对照组的67％和58％,P<0.05)。照射加电击还使雄鼠肝微粒体细胞色素p-450浓度和MFO潘力较对照组、照射组明显下降(P<0.01),但雌性大鼠血浆性激素水平与肝功能均无明显变化。照射使睾丸线粒体、肝微粒体脂质过氧化物明显升高,而照射加电击使有关组织脂质过氧化物明显降低。这些结果说明照射与照射加电击对中年大鼠具有不同的作用特点。     

60Coγ射线全身照射后大鼠脑NOS表达变化及其与神经再生的关系

目的 研究大鼠经^60Coγ全身照射致中枢神经系统损伤后，神经再生过程中NOS表达变化规律，初步探讨NOS表达变化对神经损伤后再生的影响及意义。方法 旋转式^60Coγ射线一次性全身低剂量照射，NDP组化染色。结果 大鼠经8Gy^60Coγ射线全身照射1周后，大脑皮质、基底核、丘脑和下丘脑的大部分核团NOS呈中等强度阳性表达，照射后第4周，以上脑区NOS水平明显升高，照射后第7周NOS的阳性表达逐渐减弱，但仍高于正常水平。正常对照组大鼠除海马锥体细胞层有较强的阳性标记外，其它脑区仅有弥散的NOS弱阳性标记。结论 ^60Coγ射线全身照射致大鼠脑损伤后NOS表达增强，提示NOS可能在对应的损伤神经元结构再生和突触重建过程中发挥重要作用。     

应激对大鼠血浆内皮素与一氧化氮的影响及益气通络丹的作用

方法：采用慢性随机、可逃避电脉冲刺激大鼠足底部１０ｄ造成慢性电击应激模型。结果：慢性应激可引起大鼠血浆内皮素与一氧化氮浓度同时升高，且二者的变化具有显著正相关性；慢性应激时内皮素与一氧化氮的释放均非通过肾上腺素能β受体介导；中药复方益气通络丹可降低慢性应激大鼠血浆内皮素浓度，对慢性应激大鼠血浆一氧化氮浓度的升高无影响。结论：益气通络丹对慢性电击应激损伤有一定的对抗作用     

低剂量γ射线照射提高外周血单个核细胞IL-12分泌并降低IL-10的分泌

目的探讨低剂量γ射线照射对外周血单个核细胞(PBMC)分泌IL-10及IL-12的影响。方法分离人PBMC,经17 Gy/minγ射线照射后进行体外培养。采用吖啶橙染色鉴定细胞存活情况,ELISA检测培养0、20、40、60、80 h的PBMC上清中IL-10和IL-12的水平。结果与未照射PBMC相比,低剂量γ射线照射的PBMC在体外培养24 h后,吖啶橙染色显示照射后的PBMC存活细胞略有减少;ELISA检测结果表明培养上清中IL-10含量显著降低,而IL-12含量明显增加。结论低剂量γ射线照射PBMC可引起IL-12水平升高、IL-10水平降低。     

长期电击对19月龄大鼠血浆性激素水平肝功能和脂质过氧化作用的影响

19月龄的雄性Wistar大鼠给予随机电击,平均1次/2min,每次持续0.6s,每天电击12h,持续25天,电流强度由1.0mA逐渐增加到9.5mA。长期电击使肾上腺指数明显升高(为对照组的223%,P<0.001)。对照组雄性大鼠的血浆睾酮(T)、雌二醇(E_2)水平分别为1.63±1.35ng/ml、6.36±3.25pg/ml((?)±SD,n=5)。长期电击使血浆T水平有所降低、血浆E_2水平明显升高(23.6±13.3pg/ml,(?)±SD,n=5,P<0.05),以致T/E_2比值明显下降(P<0.05)。长期电击使大鼠肝微粒体混合机能氧化酶(MFO)活力明显下降(1.03±0.10μg甲醛/mg蛋白/20min,(?)±SD,n=5,为对照组的44.5%,P<0.001)。长期电击后19月龄的雄性大鼠大脑皮层匀浆和线粒体、下丘脑匀浆以及肝微粒体的过氧化脂质(TBA反应测定)明显升高(P<0.05)。以上结果说明长期电击明显加速了19月龄的雄性大鼠的衰老过程。     

低剂量γ射线辐照外周血单个核细胞对细胞因子表达的影响

目的:探讨低剂量辐射对外周血单个核细胞细胞因子表达的刺激效应.方法:人外周血单个核细胞采用1 Gyγ射线照射,吸收剂量率为17 Gy/min,并在培养过程中不同时间采用ELISA方法检测上清液中IL-2、TNFα及IFN-γ含量.结果:经γ射线照射24 h后培养上清中IL-2、TNFα及IFN-γ含量明显升高,与对照组比较有明显差异(P<0.05),并随培养时间延长,各细胞因子含量会进一步升高.结论:低剂量辐射对外周血单个核细胞中IL-2、TNFα及IFN-γ表达具有刺激效应.     

菊藤胶囊对应激大鼠血压、血浆血管紧张素Ⅱ和血液流变学的影响

目的观察中药复方菊藤胶囊对慢性应激性高血压大鼠血压、血浆血管紧张素Ⅱ（AngⅡ）及血液流变学的影响。方法大鼠随机分为6组（每组7只）：应激＋蒸馏水组（model），应激＋菊藤胶囊高剂量组（JT—H），应激＋菊藤胶囊中剂量组（JT—M），应激＋菊藤胶囊低剂量组（JT—L），应激＋卡托普利组（captopril），正常对照组（control）；除正常对照组外，其余5组均采用低频低压交流电间断电击法。电击大鼠足底28d，制作应激性高血压模型，同时各组均加入不同的干预。后应用经尾动脉测量血压和心率，酶联免疫吸附法（ELISA）检测大鼠血浆血管紧张素Ⅱ，血液流变学和细胞流变学的各项指标。观察比较菊藤胶囊不同剂量组、卡托普利组对应激致大鼠血压及相关指标的影响。结果与正常对照组相比，模型组大鼠血压和血浆血管紧张素Ⅱ含量明显升高（P〈0．01）。全血黏度、血浆黏度、纤维蛋白原及红细胞聚集指数均明显升高（P〈0．05），红细胞变形指数无变化。与模型组相比，菊藤胶囊高、中组均能抑制应激大鼠的血压及血浆血管紧张素Ⅱ含量的升高（P〈0．01），菊藤胶囊高剂量能明显改善应激大鼠的血液流变性（P〈0．05），低剂量组应激大鼠的血液流变学无明显改变（P〉0．05）。结论菊藤胶囊能够降低应激性高血压大鼠的血压，其机理可能是通过降低血浆中血管紧张素Ⅱ的含量和改善血液流变和细胞流变性实现的。     

低剂量γ射线辐照对血清一氧化氮及一氧化氮合酶水平的影响

目的：观察低剂量γ射线照射人离体外周血对血清中一氧化氮（NO）和一氧化氮合酶（NOS）水平的影响。方法：采集10份健康献血员全血，肝素抗凝，然后采用γ射线照射，照射剂量率为17Gy／min，总吸收剂量为1Gy，分别于照射前及照射后1h，2h采用分光光度法检测血清中NO含量和NOS活性。结果：经γ射线照射1h后，血清中NO及NOS水平与照射前比较明显升高（P〈0.01）；照射后2h，血清中NOS水平与照射后1h比较无统计学差异（P〉0、05），但是还明显高于照射前的水平（P〈0．01）；在照射后2h，血清中NO含量与照射后1h比较明显降低（P〈0.01），但仍明显高于照射前水平（P〈0．01）。结论：采用剂量为1Gy的γ射线照射外周血，可引起血清中NO水平及NOS活性的显著升高．从而为低剂量辐照自体血回输对肿瘤的辅助治疗提供了理论支持。     

低水平辐射对大鼠血浆和某些腺体中cAMP和cGMP水平的影响

本研究分二批进行,第一批用成年雄性大鼠每天接受X射线全身照射50mGy/次和100mGy/次,剂量率为15mGy/分,6次/周,共照5周(30次),累积剂量分别为1.5Gy和3.0Gy。受照大鼠睾丸重量在停照后4周内呈持续性减轻,以照射剂量大,停照时间长者,减轻最明显(相当于对照43.9%)。睾丸中cAMP含量于停照后1周升高,以100mGy组明显(P<0.01),停照后2周仍显著高于对照(P<0.05),停照后4周回降到正常较低水平。而血浆和肾上腺中cAMP和胸上腺中cGMP含量无明显变化。第二批实验动物条件与第一批相同,每天接受16.3mGy,~(60)Coγ射线全身照射,剂量率为45.3pGy/分,6次/周,每次照射6小时,在照射6、10、14、18、22周,累积剂量分别为0.59、0.98、1.37、1.76、2.15Gy时与相应对照组比较,垂体、睾丸中cAMP含量及睾丸重量无显著差别,证实慢性小剂量全身照射对睾丸组织的损伤主要取决于剂量率大小,剂量率愈大损伤愈明显。     

低剂量γ射线辐照对人红细胞免疫功能和血清抗氧化酶活性的影响

目的：观察低剂量γ射线对人红细胞免疫功能和血清抗氧化酶活性的影响。方法：10份人全血，采用γ射线照射，照射剂量为1Gy，并分别于照射前及照射后1h，2h检测红细胞C3b受体花环（RBC—C30bRR）、红细胞免疫复合花环（RBC—ICR）及肿瘤红细胞花环率（RTRR）的变化情况及血清中超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GSH—Px），谷胱甘肽还原酶（GR）及过氧化氢酶（CAT）的活性。结果：人红细胞经γ射线照射后，RBC—C3R及RTRR较照射前明显升高（P〈0．05），而RBC—ICR无明显变化（P〉0．05）。经γ射线照射1h后，SOD，GSH—Px，GR及CAT活性与照射前比较明显升高（P〈0.1），照射后2h，除SOD外，所有指标与照射后1h比较进一步升高（P〈0．05）。结论：人红细胞在体外经低剂量γ射线照射后，可明显增强红细胞的免疫功能和明显提高血清抗氧化酶活性，即可诱导红细胞免疫和抗氧化酶的兴奋效应。     

Expression of TNF-alpha and TGF-beta 1 in the rat brain after a single high-dose irradiation

Cytokines and growth factors are important regulatory proteins controlling the growth and differentiation of normal and malignant glial cells. In this study, we investigated the expression and origin of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) in the subacute brain injury after a single high-dose irradiation using 60 Sprague-Dawley rats. The right cerebral hemispheres of rats were exposed to a single 10 Gy dose of gamma rays using Ir-192. The radiation effect was assessed at 1 week, 2 weeks, 4 weeks, 6 weeks, and 8 weeks after irradiation, and the results were compared with those in sham operation group. Histological changes characteristic of radiation injury were correlated with the duration after the single dose irradiation. The loss of cortical thickness also increased with the lapse of time after irradiation. The TNF-alpha expression in the irradiated cerebral hemispheres was significantly increased compared with that in the sham operation group. TGF-beta 1 expression was also increased in the irradiated hemispheres. Immunohistochemical study revealed that TGF-beta 1 was expressed predominantly by infiltrating macrophages and astrocytes around the necrotic areas. These findings indicate that TNF-alpha and TGF-beta 1 may play prominent roles in the radiation injuries after a single high-dose irradiation.     

Effects of neonatal administration of vasopressin on cardiac and behavioral responses to emotional stress in adult male rats.

Arginine-8-vasopressin (AVP) was administered subcutaneously on postnatal days 3-7 in a high (10 micrograms/100 g b.wt.) or a low dose (1 microgram/100 g b.wt.) to male Wistar rats. Control pups were untreated or saline injected. Behavioral observations in a complex maze after maturation indicated that neonatal administration of AVP increases exploratory behavior in this novel environment in a dose-dependent way. Cardiac monitoring during the conditioned emotional stress of fear of inescapable electric footshock showed that only the high dose of AVP attenuates the bradycardiac stress response. The analysis of cardiac responses also suggested an adult hyposensitivity to AVP in rats treated neonatally with AVP. In addition, the low dose of neonatal AVP was impairing the retention of a passive avoidance behavior. The data indicate that the neonatal administration of AVP exerts long-term effects upon the behavioral adaptation to novelty and memory processes related to emotional stress. That neonatal AVP is less effective in influencing adult vagally mediated cardiac stress responses suggests differences in the developmental sensitivity ("critical periods") of the central vasopressinergic systems involved in the regulation of behavior and autonomic functioning.     

脂联素和脂联素受体1在不同病程糖尿病大鼠心肌缺血预适应中的变化

目的:探讨脂联素(APN)和脂联素受体1(Ad-R1)在不同病程糖尿病大鼠离体心肌缺血再灌注(IR)损伤和缺血预适应(IPC)保护作用中的变化。方法:分别用链脲佐菌素和高脂饮食+链脲佐菌素制备1型糖尿病(TIDM)和2型糖尿病(T2DM)大鼠模型,并分别分为4周和8周2个病程组,采用Langendorff法建立离体心脏灌流模型,每组进一步分为正常对照(Con)组、IR组和IPC组3个亚组,检测冠脉流出液中乳酸脱氢酶(LDH)及肌酸激酶(CK)活性,采用ELISA法检测血清和心肌组织APN水平,采用Western blot法检测心肌组织Ad-R1蛋白表达,测定心肌梗死面积,透射电镜观察心室乳头肌超微结构,并比较上述指标在各组中的差异。结果:与对应的IR组相比,4周时IPC组LDH和CK活性显著降低(P0.01),心肌梗死区域面积明显减少,而8周时DM组的各项检测指标无明显改变。血清APN含量在糖尿病大鼠减低,尤以T2DM降低为甚(P0.05),正常大鼠心肌组织APN含量和Ad-R1表达水平在Con、IR和IPC组之间无差异;T1DM模型大鼠心肌组织APN含量在各亚组间无变化,4周和8周心肌组织Ad-R1表达量IR组较Con组明显增加(P0.01),IPC组较对应IR组Ad-R1表达量降低(P0.01);T2DM模型大鼠心肌组织APN含量4周和8周的IR组较Con组明显减少(P0.05),IPC组较对应IR组,4周组的APN显著升高,8周组无显著差异,心肌Ad-R1表达量4周和8周的IR组较Con组明显增加(P0.05),4周的IPC组较对应IR组Ad-R1表达量降低(P0.05),8周的IPC组较对应IR组Ad-R1表达量无改变。结论:T1DM和T2DM模型大鼠4周组存在IPC保护作用,8周组IPC保护作用基本消失;心肌组织APN和Ad-R1可能参与了T2DM大鼠的IPC保护作用。     

延胡索乙素对大鼠急性放射性肺损伤的保护作用

目的:探讨延胡索乙素(dl-tetrahydropalmatine,THP)对大鼠急性放射性肺损伤(irradiation induced lung injury,RILI)的保护作用.方法:成年雌性SD大鼠随机分为4组,对照组、单纯照射组(R组)、R+THP组、THP组.R组采用x射线右侧胸部单次照射15 Gy,于照射后1,4,8,12,16周分别处死大鼠,取肺组织行TUNEL及电镜检测凋亡,HE染色观察病理变化,部分肺组织行超氧化物歧化酶(superoxide dismutase,SOD)及丙二醛(malondialdehyde,MDA)检测,ELISA法测定大鼠血清TGF-p1.结果:对照组及THP组大鼠肺组织均无炎症反应.受照射组(R组、R+THP组)在照射后4～16周均表现出不同程度的肺组织细胞凋亡及RILI病理变化;但R+THP组较R组炎症反应明显减轻,R+ THP组与同时段的R组比较:肺组织中MDA水平明显降低、SOD水平明显升高,血清中TGF-p1明显降低,炎性细胞募集较少.两组间不同时段血清中TGF-p1水平、肺组织中MDA,SOD水平以及肺组织细胞的凋亡指数均有显著性差异(P＜0.05或P＜0.01).结论:THP能通过抑制凋亡、减轻氧化损伤、抑制TGF-p1等作用减轻大鼠急性RILI.     

Enhancement of hepatocarcinogenesis initiated with diethylnitrosamine or N-nitrosobis(2-hydroxypropyl)amine by a choline-deficient, L-amino acid-defined diet administered prior to the carcinogen exposure in rats.

Effects of pre-administration of a choline-deficient, L-amino acid-defined (CDAA) diet on hepatocarcinogenesis initiated with diethylnitrosamine (DEN) or N-nitrosobis(2-hydroxypropyl)amine (BHP) in rats were investigated. A pre-administrating period was set as 1 week, because CDAA diet induces liver injuries by this time-point. In a time-course study, male Fischer 344 rats, 6 weeks old, received a 1-week pre-administration of choline-supplemented, L-amino acid-defined (CSAA) or CDAA diet, DEN at a dose of 100 mg/kg body weight by a single intraperitoneal injection, then CSAA or CDAA diet for up to 8 weeks, and were sacrificed 4, 6 and 8 weeks after DEN. CDAA diet administered only after DEN significantly increased the numbers of glutathione S-transferase placental form (GST-P)-positive lesions 4, 6 and 8 weeks after DEN and their sizes 6 and 8 weeks after DEN. CDAA diet administered both before and after DEN similarly increased the numbers and sizes of GST-P-positive lesions, but with a significantly greater degree than obtained by the diet administered only after DEN. In a dose response study, rats received vechicle or DEN, at a dose of 0.001, 0.01, 0.1, 1, 10, 20, 50, 100 or 200 mg/kg body weight, 1 week after the commencement of CSAA or CDAA diet, and sacrificed 8 weeks after vehicle or DEN. The significant increases of the numbers of GST-P-positive lesions were obtained after 50-200 mg/kg body weight of DEN under the CSAA diet administration, whereas those were detected after 10-200 mg/kg under CDAA diet administration. Sizes became significantly larger with only 200 mg/kg body weight of DEN in the CSAA case but with 50-200 mg/kg in the CDAA case. Male Wistar rats received a 1-week pre-administration of CSAA or CDAA diet, vehicle or BHP, at a dose of 600 or 1200 mg/kg body weight, by a single intraperitoneal injection, then CSAA or CDAA diet for 8 weeks, and were then sacrificed. The numbers of GST-P-positive lesions demonstrated significant increment with 1200 mg/kg body weight of BHP by CDAA diet administered only after BHP and, to a significantly greater degree, by the diet administered both before and after BHP. While CDAA diet administered only after BHP did not alter the sizes of GST-P-positive lesions, the diet administered both before and after 600 and 1200 mg/kg body weight of BHP significantly increased the sizes of the lesions. These results indicate that the pre- plus post-administration of CDAA diet enhances hepatocarcinogenesis initiated with DEN or BHP, more than the post-administration only, thus providing a sensitive model to detect weak liver carcinogenic potency of environmental chemicals.     

γ射线低温辐照对胶原膜体外稳定性和细胞相容性的影响

低温下,胶原膜经γ射线辐照改性,采用剂量率为22 KG y/h,辐照剂量分别为15、25、35 KG y。测定辐照前后胶原膜抗胶原酶酶解能力,对胶原膜的体外稳定性进行了初步评价,结合红外光谱分析对辐照改性机理进行了探讨。结果表明,在实验所设计的条件下,辐照改性后胶原膜的交联度及稳定性均增加。采用M TT法结合扫描电镜观察,对辐照后胶原膜的细胞相容性进行了研究,表明在一定的辐照剂量范围内(<25 KG y),辐照对胶原膜的细胞相容性没有明显的影响。当超过一定剂量后,辐照改性将在一定程度上影响胶原膜的细胞相容性。     

组蛋白去乙酰化酶8对肾性高血压大鼠心肌肥大的影响

目的: 研究组蛋白去乙酰化酶8(histone deacetylase 8,HDAC8)在肾性高血压大鼠左心室肥厚中的表达变化及HDAC抑制剂丙戊酸钠(valproic acid sodium, VPA)对心肌肥厚的影响。方法: 建立2肾2夹肾性高血压大鼠模型,术后4周开始给药,VPA高剂量(400 mg·kg^-1·d^-1)组及VPA低剂量(200 mg·kg^-1·d^-1)组连续腹腔注射VPA给药4周,同时设立假手术组和阳性对照坎地沙坦(10 mg·kg^-1·d^-1)组,实验结束时测量左心室/体重比值,HE染色检测心肌组织形态学变化, RT-PCR检测心房利钠因子(atrial natriuretic factor,ANF)和HDAC8 mRNA表达,Western blotting检测HDAC8的表达情况。结果: HDAC8 mRNA和蛋白表达水平在肾性高血压大鼠心肌组织中明显上调;VPA能够剂量依赖性降低HDAC8的表达, 同时VPA治疗组与坎地沙坦组高血压大鼠的左心室肥厚得到明显逆转,表现为心室体重比降低, 肥大心肌形态明显改善且ANF的表达下调。结论: HDAC8参与了肾性高血压大鼠心肌肥厚的发病过程,VPA可以下调其表达并部分逆转心肌肥厚。     

Effects of irradiation on diabetes in the BB/Wor rat

Lymphoid irradiation is known to prevent spontaneous autoimmune diabetes in susceptible BB rats. The present studies investigated further the effects of radiation in diabetes prone (DP) and resistant (DR) BB/Wor rats, and histocompatible Yoshida (YOS) rats. Single doses of total body gamma irradiation (125-600 rads) induced diabetes within 22-44 days in 20 of 102 (20%) 30 day old DR rats, less than 1% of which develop the disease. Radiation was also associated with (1) a reduction in the ratio of W3/25+ to OX8+ peripheral blood lymphocytes within 2 weeks, and (2) a decreased percentage of lymph node cells expressing the RT6.1 surface alloantigen 3-4 weeks after treatment. Similar doses of irradiation did not alter the frequency or age at onset of diabetes in DP rats, and did not induce diabetes in YOS rats. When a single dose of 250 or 500 rads of gamma irradiation was followed by injection of mitogen activated spleen cells from acutely diabetic rats to adoptively transfer diabetes, 16 of 19 (84%) DR and 8 of 14 (57%) YOS rats became diabetic. Long term exposure to ultraviolet irradiation (UVB) did not alter the frequency or age at onset of diabetes in either DP or DR rats. We conclude that there may exist a population of regulatory cells relatively sensitive to gamma irradiation that play a role in determining the susceptibility of rats to autoimmune diabetes mellitus.     

Effects of Irradiation on Diabetes in the BB/WOR Rat

Lymphoid irradiation is known to prevent spontaneous autoimmune diabetes in susceptible BB rats. The present studies investigated further the effects of radiation in diabetes prone (DP) and resistant (DR) BB/Wor rats, and histocompatible Yoshida (YOS) rats. Single doses of total body gamma irradiation (125–600 rads) induced diabetes within 22–44 days in 20 of 102 (20%) 30 day old DR rats, < 1% of which develop the disease. Radiation was also associated with (1) a reduction in the ratio of W3/25⁺ to OX8⁺ peripheral blood lymphocytes within 2 weeks, and (2) a decreased percentage of lymph node cells expressing the RT6.1 surface alloantigen 3–4 weeks after treatment. Similar doses of irradiation did not alter the frequency or age at onset of diabetes in DP rats, and did not induce diabetes in YOS rats. When a single dose of 250 or 500 rads of gamma irradiation was followed by injection of mitogen activated spleen cells from acutely diabetic rats to adoptively transfer diabetes, 16 of 19 (84%) DR and 8 of 14 (57%) YOS rats became diabetic. Long term exposure to ultraviolet irradiation (UVB) did not alter the frequency or age at onset of diabetes in either DP or DR rats. We conclude that there may exist a population of regulatory cells relatively sensitive to gamma irradiation that play a role in determining the susceptibility of rats to autoimmune diabetes mellitus.