期刊文献+

稀土氧化钕颗粒物致大鼠肺损伤相关性研究 被引量:17

Research on lung injury caused by rare earth neodymium oxide particles in rats
原文传递
导出
摘要 目的探讨稀土氧化钕(Nd2O3)对大鼠肺损伤的影响。方法 72只无特定病原体级雄性SD大鼠随机分为对照组和低、中、高剂量组4组,Nd2O3染毒质量浓度分别为25.0、50.0、100.0 mg/kg。非暴露式气管内一次性灌注法建立大鼠肺损伤模型,分别在染毒后14、21和28 d,在体全肺灌洗法收集支气管肺泡灌洗液(BALF)对其炎症细胞进行分类计数,制作肺组织病理切片,普通光镜下观察大鼠肺组织病理学改变,收集肝脏、肾脏和脑标本并采用电感耦合等离子体质谱法测定Nd2O3水平。结果染毒后14、21和28 d肺组织病理切片显示,早期各组肺组织出现肺泡排列紊乱、肺泡间隔增宽,其间有大量炎症细胞浸润,晚期细胞性结节形成,弥漫成片;损伤程度随染毒剂量的增加及时间的推移而加重。染毒后28 d,各剂量组肺脏器系数、BALF中白细胞总数及其分类中性粒细胞、巨噬细胞和淋巴细胞均有不同程度升高(P<0.01)。染毒剂量分别与时间因素和器官因素之间、时间因素与器官因素之间均存在交互效应(P<0.01)。Nd2O3水平随染毒剂量增加而增加(P<0.01),21和28 d的Nd2O3水平分别低于14 d(P<0.01),肝脏Nd2O3水平分别高于肾脏和脑组织(P<0.01),高剂量组染毒后14 d肝脏Nd2O3水平最高。结论 Nd2O3颗粒物可致染尘大鼠发生肺损伤作用,早期以炎性损伤为主,晚期可形成细胞性结节。通过呼吸道染毒进入大鼠体内的Nd2O3颗粒物在肝脏、肾脏和脑之间进行再分配,其中肝脏中Nd2O3水平高于肾脏和脑组织。 Objective To explore the lung injury caused by rare earth neodymium oxide(Nd2O3 ) particles in rats. Methods Seventy-two wistar rats were randomly divided into 4 experimental groups: a control group and 3 Nd2O3 treated groups (25. 0, 50. 0 and 100. 0 mg/kg). Disposable non-exposed type intratracheal perfusion was adopted to make the rat lung injury model. Fourteen, twenty-one and twenty-eight days later, bronchoalveolar lavage fluid (BALF) was collected by bronchoalveolar lavage. White blood cell (WBC) count and differential cell counts in BALF were estimated and paraffi- nembedded lung sections with HE staining was observed under light microscope. Inductively coupled plasma mass spectrometry was used to measure the Nd2O3 content in liver, brain and kidney. Results Fourteen, twenty-one and twen- ty-eight days after the Nd2O3 exposure, lung histopathology showed that the arrangement of alveolar was disordered, the alveolar interval widened by those of inflammatory cells infiltrated in the early stage of the lung injury, which was followed by the cell nodule formation and diffuse into the film. The organ coefficients, the number of WBC and the absolute number of differential ceils, including lymphocytes, neutrophils, macrophages in the BALF were elevated in Nd2O3-treated groups (P〈0. 01 ). The factorial design analysis showed that, there were interactions between dose and time factors,dose and organ factors,and time and organ factors (P 〈 0. 01 ). Nd2O3 levels increased with the increase of infected dose (P 〈 0. 01 ). The Nd2O3 levels of 21 d and 28 d less than 14 d respectively( P 〈 0.01 ). The Nd2O3 levels of liver were higher than the kidney and brain(P 〈 0. 01 ). The highest Nd2O3 level was the high dose group of 14 d after infected in liver. Conclusion Nd2O3 particles could cause lung injury to rats, mainly inflammatory injury in the early stage, cells nodules forming in the later period. Nd2O3 particles were redistributed between the rat liver, kidney and brain through respiratory tract infected. The neodymium oxide content in liver is higher than those in kidney and brain.
出处 《中国职业医学》 CAS 北大核心 2013年第5期389-393,共5页 China Occupational Medicine
基金 国家自然科学基金(81260426)
关键词 稀土 氧化钕 支气管肺泡灌洗液 白细胞 巨噬细胞 中性粒细胞 淋巴细胞 电感耦合等离子体质谱法 Rare earth Neodymium oxide Bronchoalveolar lavage fluid White blood cell Macrophage Neutrophil Lymphocyte Inductively coupled plasma mass spectrometry
  • 相关文献

参考文献17

  • 1李明勇,陈柏林,邱林,华燚,何昀,温晟,龙春兰,魏光辉.塑化剂邻苯二甲酸二(2-乙基)己酯诱导大鼠尿道下裂的研究[J].第三军医大学学报,2012,34(20):2124-2126. 被引量:5
  • 2徐峥嵘,杜海科,王世鑫,刘殿武.牛磺酸对染矽尘大鼠肺组织炎性细胞影响[J].中国职业医学,2013,40(1):15-18. 被引量:6
  • 3Cassee FR, Campbell A, Boere AJ, et al. The biological effects of subacute inhalation of diesel exhaust following addition of cerium oxide nanoparticles in atherosclerosis-prone mice [ J ]. Environ Res, 2012,115:1 -10.
  • 4角建林,李进涛,何保丽,李波,王利梅,郑红.封闭群滇南小耳猪体重和脏器重量的测定及其相关性分析[J].昆明医科大学学报,2013,34(1):32-35. 被引量:6
  • 5郝小惠,王宏丽,刘和亮,张丽,李艳辉.姜黄素对矽肺大鼠肺组织水通道蛋白-1表达影响[J].中国职业医学,2012,39(6):471-474. 被引量:7
  • 6Giri S, Karakoti A, Graham RP, et al. Nanoceria : a rare-earth nano- particle as a novel anti-angiogenie therapeutic agent in ovarian cancer [J]. PLoS One,2013,8(1):e54578.
  • 7Lee S, Hayashi H, Maeda M, et al. Environmental factors producing autoimmune dysregulation--chronic activation of T ceils caused by sili- ca exposure [ J ]. Immunobiology, 2012,217 ( 7 ) :743 - 748.
  • 8Li XF, Liao J, Xin ZQ, et al. Relaxin attenuates silica-induced pul- monary fibrosis by regulating collagen type I and MMP-2 [ J]. Int Im- munopharmacol,2013,17 ( 3 ) :537 - 542.
  • 9Zhu Z, Yang G, Wang Y, et al. Suppression of thioredoxin system contributes to silica-induced oxidative stress and pulmonary fibrogene- sis in rats [ J ]. Toxicol Lett,2013,222 ( 3 ) : 289 - 294.
  • 10van Wessem KJ, Hennus MP, van Wagenberg L,et al. Mechanical ventilation increases the inflammatory response induced by lung contu- sion[J]. JSurgRes,2013,183(1):377-384.

二级参考文献112

共引文献327

同被引文献229

引证文献17

二级引证文献61

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部