摘要
目的 探讨吸入不同浓度SO2 引起小鼠肺组织及血清中抗炎及致炎因子的变化规律 ,进一步阐明SO2致炎作用机制。方法 采用酶联免疫吸附法 (ELISA)分别检测小鼠肺组织及血清中肿瘤坏死因子 (TNF -α)、白介素- 6 (IL - 6 )、转化生长因子 - β1(TGF - β1)的含量。 结果 ( 1)肺组织 :当SO2 吸入浓度为 14mg/m3 时 ,肺组织中IL- 6、TNF -α的含量均显著升高 (P <0 0 5 ) ,而TGF - β1没有明显变化 ;吸入 2 8mg/m3 SO2 后 ,肺组织中IL - 6、TNF-α均显著升高 (分别为P <0 0 1,P <0 0 5 ) ,TGF - β1的升高不明显 ;吸入5 6mg/m3 SO2 之后 ,肺组织中 3种细胞因子均未见显著改变。 ( 2 )血清 :只有TNF -α在SO2 吸入浓度为 14mg/m3 时显著升高 ,其余实验小鼠的血清中 3种细胞因子均无显著改变。 ( 3)吸入SO2 后导致肺部致炎因子浓度升高且有明显的剂量 -效应关系 ,而抗炎因子浓度无显著改变。 ( 4 )血清中只有TNF -α在SO2 吸入浓度为 14mg/m3 时显著升高。结果表明 ,SO2 的致炎作用主要发生在肺组织 ,且与这些细胞因子有关。结论 测定肺组织细胞因子对于了解SO2
Objective To investigate the effect of sulfur dioxide inhalation on levels of pro-and anti-inflammatory cytokines in lungs and serum of mice and further to elucidate an immunotoxic mechanism of SO 2.Methods Levels of interlukin-6 (IL-6),tumor necrosis factor-α (TNF-α),transforming growth factor-β1 (TGF-β1)were measured by the enzyme-linked immunosorbent assay.Results (1)For lung tissues,exposure to SO 2 at 14 ?mg/m\+3 caused statistically significant increase of IL-6 and TNF-α levels ( P <0.05),at 28 ?mg/m\+3 caused statistically highly significant increase of IL-6 levels( P <0.01)and significant increase of TNF-α( P <0.05),at 56 ?mg/m\+3 caused no any increase of IL-6 and TNF-α levels.SO 2 at all concentrations tested could not cause significant changes of TGF-β1 in lung.(2)For serum,SO 2 at all concentrations tested could not cause significant changes of IL-6,TNF-α and TGF-β1 levels,except TNF-α at 14?mg/m\+3 of SO 2.Conclusion (1)The levels of pro-inflammatory cytokines in lungs were increased in a dose-dependent manner after exposure to SO 2,but anti-inflammatory cytokine had no significant difference.(2)In serum,levels of the three cytokines had no significant differences between SO 2 exposure and control groups,except TNF-α at 14?mg/m\+3 of SO 2.These results implied that inflammation reaction could be induced in lung tissue by SO 2 inhalation and the inflammation reaction might relate to these cytokines.And determination of cytokines in lung may be more valuable than in serum when lung injury was caused by SO 2.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2004年第9期1050-1051,共2页
Chinese Journal of Public Health
基金
国家自然科学基金(30 0 70 647
30 2 30 31 0)
山西省自然科学基金