期刊文献+

大鼠百草枯中毒肺内炎症因子表达 被引量:4

The expression of pulmonary inflammatory factor in paraquat poisoning rats
下载PDF
导出
摘要 目的:测量百草枯中毒后大鼠血清中炎症因子的水平。方法:将96只大鼠随机分为阴性对照组、高剂量染毒组(120mg/kg)、中剂量染毒组(60mg/kg)和低剂量染毒组(30mg/kg),每组24只大鼠。实验分8、24、72h三个时间段进行观察。应用酶联免疫吸附法(ELISA)测量血清TGF-β1、TNF-a、IL-10浓度。将大鼠肺进行病理切片及Masson染色观察肺纤维化情况。结果:随染毒时间延长,各剂量组细胞因子水平逐渐增加,24、72h组与对照组比较均有显著性差异(P<0.05)。72h高剂量组各指标与同时间点低剂量组比较均有显著性差异(P<0.05)。72h高、中、低3个剂量组与8h时间点比较有显著性差异(P<0.05)。大鼠肺组织中出现炎性粒细胞浸润,广泛弥漫的间质纤维化表现。Masson染色,24h后肺组织中分泌纤细的胶原纤维,72h后可见到大量蓝染的胶原纤维。结论:大鼠百草枯中毒后TGF-β1、TNF-a、IL-10等炎症因子水平显著升高。 Objective: To measure serum levels of inflammatory factors in paraquat poisoned rats. Meth- ods: 96 rats were grouped in accordance with the randomly principle. They were divided into control group and high dose exposure group (120mg/kg), middle dose exposure group (60mg/kg) and low-dose exposure group (30mg/ kg), n= 24 rats. Experimental were divided into8,24,72 h points for observation. Used enzyme linked immunosor- bent assay (ELISA) measurement to measure serum TGF-β1 , TNF-a, IL-10 concentration. The rats lung were used biopsy and Masson staining to observe pulmonary fibrosis. Results: With the exposure time, each dose group the levels of eytokines gradually increased. 24,72 h compared with the control group, the differences were statistically significant (P〈0.05 orP〈0.01). The every target in 72h high dose group with the same point compared with low- dose group was significantly (P〈0.05). 72h high, medium and low-dose group compared with the 8h time group was statistically significant (P〈0. 05). Rat lung tissue infiltration appears inflammatory granuloeytes, extensive diffuse interstitial fibrosis of the performance. Conclusion: In paraquat poisoned rats, theinflammatory cytokine of TGF-β1 , TNF-a, IL-10 levels were significantly increased.
出处 《陕西医学杂志》 CAS 2012年第9期1107-1109,共3页 Shaanxi Medical Journal
基金 陕西省科学技术研究发展计划项目(No 2012k16-01-03)
关键词 中毒/病理生理学 炎症趋化因子类/代谢 动物 实验 大鼠 Poisoning/physiopathology Chemokines/metabolism Animals,laboratory Rats
  • 相关文献

参考文献2

二级参考文献19

  • 1陈莹,董静,陈杰.γ-干扰素对矽肺大鼠肺脏白介素-4和转化生长因子-β_1蛋白表达的影响[J].中华劳动卫生职业病杂志,2004,22(5):350-353. 被引量:7
  • 2李海潮,Chin Med J,1996年,109卷,533页
  • 3Holmes A;Abraham DJ;Susan S.CTGF and SMADs,Maintenance of sclerpderma phenotype is independent of SMADs signaling[J],2001(14).
  • 4Nakao A;Fujii M;Matsumura R.Transient gene transfer and expression of Smad7 prevents bleomycin induced lung fibrosis in mice[J],2001(01).
  • 5Wang Q;Wang Y;Hyde DM.Reduction of bleomycin induced lung fibrosis by transforming growth factor β soluble receptor in hamsters[J],2000(90).
  • 6Welsh DA;Summer WR;Dotard EP.Keratinocyte growth factor prevents ventilator-induced lung injury in ex vivo rat model,2000.
  • 7Vivekananda J;Awasthi V;Awasthi S.Hepatocyte growth factor is elevated in chronic lung injury and inhibits surfactant metabolism,2000(02).
  • 8Geraldine AF;Victor JT;Barry LF.Transforming growth factor-betal-induced activation of the EPK pathway/activator protein-1 in human lung fibroblasts requires the autocrine induction of basic fibroblast growth factor[J],2000(36).
  • 9Lee TC;Gold LI;Reibnian J.Immunohistochemical localization of transforming growth factor beta and insulin-like growth factor I in asbestosis in the sheep model[J],1997(03).
  • 10Maeda A;Hiyama K;Yamakido H.Increased expression of platelet derived growth factor A and insulin-like growth factor I in BAL cell during the development of bleomycin induced pulmonary fibrosisinmice[J],1996(03).

共引文献27

同被引文献59

引证文献4

二级引证文献36

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