期刊文献+

不同程度风邪对小鼠肺脏病理改变及炎性因子的影响 被引量:3

Effects of Different Levels Wind Evil on Pathological Changes of Mice's Lung and Inflammatony Cytokines
下载PDF
导出
摘要 目的:探讨不同程度风邪对小鼠肺脏病理改变及肺组织匀浆中肿瘤坏死因子-α及白细胞介素-1β水平变化的影响,旨在说明风邪与肺脏损伤之间存在量的相关性。方法:24只小鼠随机分为空白组(KB)、2级风力组(W2)、4级风力组(W4),每组8只,置于不同的风力环境中进行饲养。4天后,光镜下观察小鼠肺组织及气道病理改变,酶联免疫吸附法检测肺组织匀浆TNF-α、IL-1β含量。结果:与空白对照组比较,各风力组小鼠肺脏均出现不同程度的病理改变及细胞因子含量的变化;各风力组小鼠肺脏TNF-α及IL-1β含量均明显增加(P<0.01),且W4组较W2组的细胞因子含量增加明显(P<0.01)。结论:风邪会引起肺脏病理改变和炎性因子含量的增加,且随着风邪程度的增加,肺脏损伤趋于严重;当风速达到7m/s且刺激时间达到2小时,部分肺组织会出现化脓性病变。 Objective: To explore effects of different levels wind evil on lung pathological changes and tumor necrosis factor α and interleukin 1β in lung homogenate,in order to illustrate the correlation between wind and lung injury. Methods: 24 mice were divided into blank group( KB),grade 2 wind group( W2) and grade 4( W4) wind group by random number table method,each group contained eight mice,they were put in different wind environment,then the pathological changes of lung tissue of mice and airway were observed,enzyme-linked immunosorbent assay to detect in the contents of TNF-α,IL-1β in lung tissue homogenate. Results: To compare with the control group,different degrees of pathological changes were appeared and there was obvious difference on several cytokines in the three groups,TNF-α and IL-1β were significantly increased( P〈0. 01),and cytokines of W4 group increased mone significantly than those in control( P〈0. 01). Conclusion:Wind evil can cause lung pathological changes and the increasing of the content of inflammatory factor levels,which was with the increaseing of the degree of the wind,the more severe lung injury; When the wind speed reaches 7 m / s and stimulation for 2 hours,some will appear suppurative lung tissue lesions.
出处 《中国中医药科技》 CAS 2014年第6期601-603,共3页 Chinese Journal of Traditional Medical Science and Technology
基金 "泰山学者"建设工程专项经费资助No.ts20110819 山东省科技发展计划No.2011GGH21811
关键词 风邪 肺脏病理 炎性因子 小鼠 wind evil pathological change of lung inflammatory cytokines mice
  • 相关文献

参考文献4

二级参考文献23

共引文献41

同被引文献65

引证文献3

二级引证文献47

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