共查询到19条相似文献,搜索用时 78 毫秒
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探讨小剂量重复照射下大鼠血清转化生长因子-β(TGF-β)和肿瘤坏死因子-α(TNF-α)的变化,及其用于检测放射性肺损伤的可能性.64只Wistar大鼠随机分为对照组(32只)和照射组(32只),后者用直线加速器对大鼠右肺进行分次照射(3Gy/次,2次/w,累积剂量为30Gy),于照射后第5、8、12和26w分别对两组大鼠(各8只)取静脉血用RIA测定TGF-β、TNF-α.结果表明照射组大鼠不同时相血清TGF-β、TNF-α水平低于对照组,其中TGF-β在8w(P<0.01)及12w(P<0.05)明显低于对照组,TNF-α在5w明显低于对照组(P<0.05).在小剂量重复照射过程中,血清TGF-β、TNF-α水平的变化,可能作为放射性肺损伤的监测指标之一. 相似文献
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目的探讨一氧化氮和内皮素-1在缺氧时对心肌血流量的调节作用。方法大鼠随机分为平原组和急性缺氧组,用99mTc标记蟾蜍红细胞测定心肌血流量,用Gess法和放免法分别测量血浆和心肌NO2-、内皮素-1(endothelin-1,ET-1)含量,用双波长分光光度法测量一氧化氮氧合酶(nitric oxide synthase,NOS)活性。结果急性缺氧导致左右心室心肌血流量、血浆和心肌血NO2-、ET-1含量、NOS活性明显增高(P〈0.05),左右心室心肌血管阻力和心肌ET-1/NO2-比值明显下降(P〈0.05),血球压积(Hct)及心室重量指数无明显变化。结论急性缺氧时,左右心室心肌血流量增加,ET-1/NO参与了急性缺氧时心肌血流量的调节,以NO的扩血管作用为主。 相似文献
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内皮素-1对大鼠血管平滑肌表型转化和增殖的影响 总被引:5,自引:2,他引:3
目的:通过内皮素-1作用于大鼠血管平滑肌细胞(VSMC)及对内皮素-1受体信号的阻断,探讨内皮素-1对VSMC表型转化和增殖的影响及机制.方法:取大鼠主动脉贴块培养VSMC,用内皮素-1及其受体阻断剂BQ123分别作用于一般培养的VSMC和血清饥饿培养的VSMC.用BrdU标记细胞增殖;RT-PCR检测高血压相关基因-1(HRG-1)和SM22α表达变化.结果:内皮素-1作用后VSMC增殖显著增多,HRG-1和SM22α mRNA在一般培养和饥饿培养的VSMC中表达均明显减少;而加入阻断剂BQ123后增殖细胞大大减少,HRG-1和SM22α mRNA表达明显上调.结论:内皮素-1有促进VSMC增殖作用并可使VSMC从收缩型向合成型转化,并且内皮素-1对VSMC的作用是不可逆的;受体信号途径是内皮素-1对VSMC表型转化和增殖作用的机制之一. 相似文献
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目的 探讨胰岛素样生长因子-1(IGF-1)及内皮素-1 (ET-1)与胎儿宫内发育受限(FGR)发病的关系.方法 应用放射免疫分析法和酶联免疫吸附试验,分别测定21例FGR患儿脐血、孕妇(FGR组)血清及羊水中IGF-1和ET-1水平,同期住院的正常晚期妊娠妇女34例(正常妊娠组)作为对照.结果 (1)FGR组孕妇血清IGF-1为112.16±7.02μg/L,低于正常妊娠组的207.07±8.25μg/L,两者比较,差异有显著性(P<0.01);FGR组脐血清IGF-1为16.27±7.38μg/L,低于正常妊娠组的44.89±6.44μg/L,两者比较, 差异有极显著性(P<0.001);FGR组羊水中IGF-1 与正常妊娠组无明显差异(P>0.05);(2)FGR组脐血清ET-1为79.34±3.67μg/L,高于正常妊娠组的43.96±4.16μg/L,两者比较,差异有显著性(P<0.01);FGR组羊水中ET-1水平(21.96±1.89μg/L)明显高于正常妊娠组(10.41±2.13μg/L),两组相比有显著差异(P<0.01);而FGR组孕妇血清ET-1与正常妊娠组相比无明显差异(P>0.05).结论 IGF-1及ET-1在FGR的发病中可能起到重要作用有关. 相似文献
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巨噬细胞浸润及细胞间粘附分子-1表达在油酸致大鼠急性肺损伤发病中的作用 总被引:3,自引:3,他引:0
目的:探讨巨噬细胞浸润及细胞间粘附分子-1(ICAM-1)表达在油酸诱导的大鼠急性肺损伤(ALI)中的作用。方法:雄性Wistar大鼠静脉注射油酸复制ALI为油酸组,静脉注射生理盐水为对照组。静注后4h,测定血气(左心PaO2)、肺泡通透指数等肺损伤指标。支气管肺泡灌洗液(BALF)中巨噬细胞比和可溶性细胞间粘附分子-1(sICAM-1)水平。用原位杂交检测ICAM-1mRNA表达水平和免疫组化双重套染方法检测巨噬细胞浸润程度与ICAM-1表达的关系。结果:油酸组PaO2低于对照组、肺泡通透性指数高于对照组(P<0.01),BALF中巨噬细胞比例,sICAM-1水平显著高于对照组(P<0.01)。油酸组肺组织ICAM-1表达明显高于对照组,且肺组织中巨噬细胞浸润数、ICAM-1表达水平和肺损伤指标呈显著正相关。结论:巨噬细胞浸润在油酸致急性肺损伤中起重要作用,ICAM-1参与介导了巨噬细胞对组织的粘附、浸润和ALI的发生发展。 相似文献
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目的 探讨内皮素-1(ET-1)介导循环间歇性低氧(CIH)影响颈动脉体可塑性的潜在分子机制。 方法(1)动物实验:将32只雄性SD大鼠随机分为2组,常氧对照组(Con)和循环间歇性低氧模型组(CIH),每组16只。模型制作21d后,将每组(Con和CIH)16只大鼠再分为2组,分别予尾静脉注射ET-1(1×10-6 mol/kg体重)或按照上述剂量计算的等体积生理盐水。30 min后,收集颈动脉体,采用Western blotting检测相关信号通路分子蛋白水平的变化。(2)器官培养:离体培养颈动脉体组织,ET-1(1×10-4 mol /L)处理不同时间(0 min、10 min、60 min),通过Western blotting检测p38丝裂原活化蛋白激酶(p38 MAPK)磷酸化水平。 结果 (1)CIH上调颈动脉体内皮素受体A(ET-A)和ET-B蛋白的表达;(2)与其他各组相比,ET-1可显著上调CIH大鼠颈动脉体磷酸化蛋白激酶A(p-PKA)、p-p38 MAPK、磷酸化的钙调蛋白激酶Ⅱ(p-CaMKⅡ)、磷酸化的环磷腺苷效应元件结合蛋白 (p-CREB)磷酸化水平和RhoA蛋白表达水平;(3)ET-1上调离体器官培养的颈动脉体p-p38 MAPK磷酸化水平,10 min较60 min明显。 结论 ET-1可能通过PKA/p38 MAPK/CaMKⅡ/CREB和RhoA信号通路调控CIH诱导的颈动脉体可塑性。 相似文献
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目的 探讨内皮素-1(ET-1)在烫(烧)伤大鼠脑血管损伤的表达及其作用。方法应用组织学方法观察8只烫伤大鼠脑基底动脉组织结构的变化;应用RT-PCR测定48只烫伤大鼠脑基底动脉ET-1 mRNA的表达;应用Western blotting分析48只烫伤大鼠脑基底动脉ET-1的表达;应用放射免疫分析检测48只烫伤大鼠脑基底动脉ET-1 水平的变化。结果 烫伤大鼠脑基底动脉呈现病理学组织结构变化;烫伤后3h大鼠脑基底动脉ET-1 mRNA表达较正常对照组开始升高,6h 达高峰;烫伤后6h大鼠脑基底动脉ET-1 表达较正常对照组增强,12h 达高峰;烫伤后各组大鼠脑基底动脉ET-1水平较正常对照组明显升高,6h 达高峰。结论 烫(烧)伤可诱发大鼠脑血管ET-1表达增加,增加表达的ET-1可能与烫(烧)伤大鼠脑血管损伤的病理发生有关。 相似文献
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Liping Wang Jing Zhang Baozhong Wang Guifu Wang Junlong Xu 《International journal of clinical and experimental pathology》2015,8(5):4815-4822
It has been reported that HMGB1 participated in various types of lung injury. In this study, we explored whether blocking HMGB1 has a preventive effect on the early radiation-induced lung injury and investigate the mechanism. Mice model of radiation-induced lung injury were accomplished by a single dose irradiation (15 Gy) to the whole thorax. Irradiated mice were treated with HMGB1-neutralizing antibody intraperitoneally dosed 10 μg, 50 μg, 100 μg/mouse respectively and were sacrificed after one week post-irradiation. Lung tissue slices were stained by H&E, and alveolitis was quantified by Szapiel scoring system. The level of cytokines TNF-γ in bronchoalveolar lavage fluid was detected by ELISA method. And p65NF-κB, p50NF-κB protein expression in mice lung tissues was detected by Western blot analysis. The results showed that blocking HMGB1 inhibited the inflammatory response, and thereby decreased the degree of alveolitis of irradiated lung tissue. In addition, HMGB1 antagonist can restrain the expression of type Th2 or Th17 derived inflammatory cytokines TNF-α, IL-6 and IL-17A, promote the expression of Th1 type cytokines INF-γ, and inhibit p65 NF-κB but promote p50 NF-κB activation, which promoted the resolution of the radiation-induced inflammatory response. In conclusion, blocking HMGB1 can reduce the degree of early radiation-induced lung injury, and its mechanism may be related to the promotion of p50NF-κB activation and its downstream molecules expression. Inhibiting HMGB1 may be a new target to deal with early radiation-induced lung injury. 相似文献
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血红素氧合酶对大鼠肺缺血再灌注损伤的保护作用 总被引:4,自引:1,他引:4
探讨血红素氧合酶 1(HO 1)对大鼠肺缺血再灌注损伤 (I/R)的保护作用。Wistar大鼠随机分成假手术 (sham)组、I/R组、Hemin组和ZnPP IX组。采用夹闭大鼠左肺门 30min ,再灌注 12 0min ,分别观察各组HO 1活性 ,肺组织形态学变化 ,肺湿干重比、伊文思蓝含量、支气管肺泡灌洗液 (BALF)中细胞计数及蛋白含量变化。与sham组比较 ,I/R组和hemin组肺组织HO 1活性显著增高 (P <0 0 1) ,ZnPP IX组能取消hemin诱导的HO 1活性增高 (P <0 0 1)。光镜下可见I/R组和ZnPP IX组肺组织水肿 ,部分动物肺泡腔中可见出血 ,并伴有局部肺不张 ,而hemin组肺组织形态学改变明显减轻。Hemin组肺湿干重比、伊文思蓝含量、BALF中细胞数和蛋白含量均低于I/R组和ZnPP IX组 ,但仍高于sham组 (P <0 0 1)。结果提示 ,HO 1对在体大鼠肺I/R损伤具有部分保护作用 相似文献
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自发性高血压鼠脑基底动脉ET-1的表达及其意义 总被引:1,自引:0,他引:1
为探讨高血压时期内皮素-1(endothelin-1,ET-1)在脑血管神经源性调节中的作用,本研究应用反转录-聚合酶链式反应(RT-PCR)技术,检测了自发性高血压鼠脑基底动脉ET-1mRNA的表达变化;应用免疫印迹(Western blotting)方法,观察了自发性高血压鼠脑基底动脉ET-1的表达。结果显示:自发性高血压鼠脑基底动脉ET-1mRNA的表达较正常血压鼠明显增加;自发性高血压鼠脑基底动脉ET-1表达亦较正常血压鼠明显增加(P<0.05)。此结果提示自发性高血压鼠脑基底动脉高表达的ET-1和ET-1mRNA在自发性高血压鼠脑血管的神经源性调节中可能发挥重要作用。 相似文献
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Augmented expression of endothelin-1, endothelin-3 and the endothelin-B receptor in breast carcinoma 总被引:4,自引:0,他引:4
AIMS: Endothelins (ETs) are peptides expressed in many tumours which may stimulate angiogenesis and desmoplasia. Because ETs have not been extensively studied mammary neoplasia, we assessed ET protein and mRNA expression and receptor mRNA expression in normal and neoplastic breast tissues. METHODS AND RESULTS: Tissues from five normal breasts, six fibroadenomas, seven ductal carcinomas in situ (DCIS) and 25 invasive carcinomas were stained with anti-ET-1 and anti-ET-3 antibodies and analysed using a grading system. ET-1, ET-3, ETA and ETB mRNA expression was assessed by quantitative RT-PCR from eight carcinomas and five normals. Weak staining for ET-1 and ET-3 was detected in all normals. Moderate to strong staining was seen in 72% and 64% of carcinomas for ET-1 and ET-3, respectively. Most fibroadenomas showed weak positivity for ET-1 (83%) and ET-3 (67%). ET-1 and ET-3 mRNA levels were upregulated in carcinomas compared with normal breast. No ETA mRNA was not detected in any tissue. ETB mRNA was detected in normal breast and was increased in carcinomas. CONCLUSION: These results suggest that the ET system is altered in breast carcinomas and this may be of importance in the progression from in-situ to invasive carcinoma. 相似文献
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Lijuan Chen Xiufeng Hu Huijuan Wu Yongxu Jia Jie Liu Xiaoqian Mu Hongbo Wu Yanqiu Zhao 《Pathology, research and practice》2019,215(3):427-432
Validated serum biomarkers for patients suffering from non-small cell lung cancer (NSCLC) brain metastasis are urgently needed for early diagnosis, treatment monitoring, and prognostic classification in daily clinical practice. Serum S100B was reported to be a marker of leaky blood-brain barrier (BBB), which was often caused by brain tumors. This study aimed to investigate the role of S100B in NSCLC brain metastasis. The results showed that serum S100B correlated significantly with NSCLC brain metastasis (P?<?0.001). When evaluated by the ROC curve, at the cutoff point 13.83 pg/ml, the sensitivity and specificity were 94% and 93%, respectively (AUC= 0.938, P < 0.001). High level of serum S100B was significantly correlated with a higher number of brain metastases and significantly worse prognosis (P?<? 0.05). In addition, S100B was an independent prognostic factor (P?<? 0.001). In conclusion, serum S100B was a sensitive and specific marker for early detection of brain metastasis in NSCLC and could be used as a surveillance tool for prognosis evaluation. 相似文献
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<正>急性肺损伤(acute lung injury,ALI)是急危重症患者常见的一种器官损伤,肺实质细胞死亡是ALI的基础,明确细胞死亡的发生机制将为防治ALI提供重要的理论支撑[1]。细胞自噬(autophagy)是细胞代谢过程中的衰老细胞器和异常蛋白质等成分降解的过程,受多条信号通路与多种信号分子的调节,有利于维持细胞稳态;病理状态下,自噬被激活或抑 相似文献
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维甲酸降低放射性肺损伤大鼠肺组织中IL-18 mRNA及蛋白的水平 总被引:4,自引:0,他引:4
观察IL 18在放射性肺损伤大鼠肺组织的变化及维甲酸对其影响。健康雌性SD大鼠 6 0只随机分为 3组 :正常对照组 (C组 )、单纯照射组 (R组 )、维甲酸治疗组 (W组 ) ,每组 2 0只。后 2组动物行直线加速器全胸部照射 ,单次剂量 15Gy ,距离 1m ,照射面积 4.5cm× 4.5cm ,剂量率 2Gy/min ,W组维甲酸灌服剂量 2 0mg/kg ,C、R组以等量生理盐水灌服直至活杀。用免疫组化染色、原位杂交、图像分析的方法观察IL 18在放射性过程肺中的变化特点。IL 18免疫组化在照射后 30、6 0d明显增强 (P <0.0 1) ,W组 5、30、6 0d明显减弱 (P <0.0 1)。IL 18mRNA在照射后15d明显增强 (P <0 .0 5 ) ,W组 5、15、6 0d明显减弱 (P <0.0 1)。IL 18参与放射性肺损伤的发生、发展。而维甲酸无论从转录水平还是蛋白质水平都能有效抑制IL 18,为治疗放射性肺损伤提供了实验依据 相似文献
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目的:探讨内毒素血症大鼠脑底动脉内皮素-1(ET-1)能神经纤维诱发脑血管痉挛发生与发展的关系,为深入阐明内毒素血症诱发脑血管痉挛的发病机制提供形态学依据。方法:96只Wistar大鼠随机分为对照组、内毒素血症组(注射内毒素第3、6、12、24、48h),分别采用放射免疫法检测血浆内皮素-1水平的变化,采用免疫组织化学ABC法对大鼠脑底动脉内皮素-1能神经纤维进行观察。结果:内毒素血症后3、6、12h大鼠血浆内皮素-1水平较对照组明显升高(P0.05),内毒素血症后24h和48h已趋于正常(P0.05)。此外,对照组和内毒素组大鼠脑底动脉可见棕褐色,呈细线状分布的内皮素-1能免疫反应阳性纤维,其中内毒素血症后第6h和12h大鼠脑底动脉内皮素-1能神经纤维密度显著增高(P0.05)。结论:内毒素血症大鼠血浆内皮素-1水平升高,脑底动脉内皮素-1能神经纤维密度增加,提示内皮素-1参与了内毒素血症诱发脑血管痉挛的病理生理过程,为脑血管痉挛的神经-体液调节机制提出了新思路,同时为临床预防和治疗脑血管痉挛提供了理论依据。 相似文献