期刊文献+

细胞自噬在砷暴露所致肺损伤中的作用 被引量:2

Role of Autophagy in Rats Lung Injury Induced by Arsenic Exposure
在线阅读 下载PDF
导出
摘要 目的探讨细胞自噬在砷暴露所致大鼠肺损伤中的作用。方法 24只无特定病原体(SPF)级健康雄性SD大鼠随机分为4组,即对照组,砷暴露低(10μg/L)、中(100μg/L)、高(1 000μg/L)剂量组,砷暴露组通过自由饮用含Na As O2的水进行染毒,对照组自由饮用不含Na As O2的水,染毒28 d后统一处死。ELISA法测定支气管肺泡灌洗液(BALF)中TNF-ɑ、IL-6、IL-8、IL-10的含量。Western blot法检测肺组织中自噬相关蛋白NBR1、p62、LC3Ⅱ表达量。结果砷暴露组大鼠BALF中促炎因子TNF-a、IL6、IL8表达量显著高于对照组(P<0.05),且100μg/L组的IL-6最高;砷暴露1 000μg/L组的抑炎因子IL-10含量显著低于对照组(P<0.05);与对照组相比砷暴露组大鼠肺组织中p62、NBR1的表达量增加(P<0.05),且存在剂量—反应关系;与对照组相比砷暴露组大鼠肺组织中LC3Ⅱ蛋白表达量显著下降(P<0.05),且存在剂量—反应关系。结论砷暴露所致大鼠肺损伤中,细胞自噬被抑制时会加重大鼠肺部的炎症损伤,当Na As O2暴露浓度达到100μg/L时,会对大鼠肺组织造成明显的损伤。 Objectives To study the role of autophagy in the lung injury of rats induced by arsenic exposure.Methods Twenty four specific pathogen free( SPF) healthy male SD rats were randomly divided into four groups,namely the control group,the low( 10 μg / L),medium( 100 μg / L) and high( 1 000 μg / L) arsenic exposure groups. Arsenic exposure groups were intoxicated by sodium arsenite( Na As O2) in drinking water for 28 days. The level of TNF-ɑ,IL-6,IL-8 and IL-10 in bronchoalveolar lavage fluid( BALF) were determined by ELISA and the expression of NBR1,p62 and LC3 Ⅱ related to the autophagy in lung tissue were determined by Western Blot.Results The expression of proinflammatory cytokines TNF-a,IL6 and IL8 in arsenic exposure groups were significantly higher than that in the control group( P〈 0. 05). The level of IL6 in the medium arsenic exposure group( 100 μg /L) was the highest and the level of IL-10 in the high arsenic exposure group( 1 000 μg /L) was significantly lower than the control group( P〈 0. 05). Compared with the control group,the expression of p62 and NBR1 in the lung tissue of arsenic exposure groups was higher( P〈 0. 05),and there was a dose-response relationship.In contrast,compared with the control group,the expression of LC3Ⅱ in the lung tissue of arsenic exposure groups were lower( P〈 0. 05),and there was a dose-response relationship too. Conclusions The exposure of rats to arsenic would increase the inflammation of lung tissue when the autophagy was inhibited. In particular,when the concentration of Na As O2 reaching to 100 μg / L,the damage of lung tissue in rats was more severe.
出处 《环境卫生学杂志》 2015年第4期336-340,共5页 JOURNAL OF ENVIRONMENTAL HYGIENE
基金 饮用水砷污染所致肺部损伤机制的研究(内蒙古自然科学基金 项目编号:201301066)
关键词 细胞自噬 砷暴露 NBR1 LC3Ⅱ P62 autophagy arsenic exposure NBR1 LC3 Ⅱp62
  • 相关文献

参考文献19

  • 1武婧,王素华,余艳琴,高艳荣,郑姗姗,王春虾,张营,王玉,李秋玲.稀土氧化钕颗粒物致大鼠肺损伤相关性研究[J].中国职业医学,2013,40(5):389-393. 被引量:17
  • 2郭效中,刘天余.有机砷制剂对畜禽营养作用的研究进展[J].饲料研究,2000,23(1):15-17. 被引量:11
  • 3孙建新,安娟,连军.影响实验动物脏器重量及脏器系数因素分析[J].实验动物科学,2009,26(1):49-51. 被引量:92
  • 4肖静,吴顺华,郑玉建,王婷.地方性砷中毒患者细胞因子水平与抗氧化能力相关分析[J].新疆医科大学学报,2006,29(1):7-9. 被引量:11
  • 5Jones SA, Mills KH, Harris J. Autophagy and inflammatory dis- eases[Jl. Immunology and cell biology, 2013. 91 (3): 250 -258.
  • 6Levine B, Mizushima N, Virgin HW. Autophagy in immunity and inflammation[J]. Nature, 2011, 469(7330): 323-335.
  • 7Nakahira K, Haspel JA, Rathinam VA, et al. Autophagy proteins regulate innate immune responses by inhibiting the release of mi-tochondrial DNA mediated by the NALP3 inflammasome[ J]. Na- ture immunology, 2011. 12 (3) : 222 - 230.
  • 8Zhou R, Yazdi AS, Menu P, et al, A role for mitochondria in NLRP3 inflammasome activation [ J ]. Nature, 2011. 469 (7329) : 221 -225.
  • 9Zheng Y, Gardner SE, Clarke MC. Cell death, damage- associ- ated molecular patterns, and sterile inflammation in cardiovascu- lar disease[ J]. Arteriosclerosis, thrombosis, and vascular biolo- gy, 2011. 31(12) : 2781 -2786.
  • 10He C, Klionsky DJ. Regulation mechanisms and signaling path- ways of autophagy [ J ]. Annual review of genetics, 2009. 43 : 67.

二级参考文献58

共引文献128

同被引文献9

引证文献2

二级引证文献2

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