西安交通大学学报（医学版）
西安交通大學學報（醫學版）
서안교통대학학보（의학판）
Journal of Xi'an Jiaotong University (Medical Sciences)
2015年
6期
836-839
,共4页
杨宇轩%闫思琪%衣颖杰%张喆%聂雨晨%郭坤%于燕
楊宇軒%閆思琪%衣穎傑%張喆%聶雨晨%郭坤%于燕
양우헌%염사기%의영걸%장철%섭우신%곽곤%우연
PM2.5%WI-38 人胚肺细胞%基因差异表达%斑点杂交%TNF-α%IL-2%IL-6%IL-8
PM2.5%WI-38 人胚肺細胞%基因差異錶達%斑點雜交%TNF-α%IL-2%IL-6%IL-8
PM2.5%WI-38 인배폐세포%기인차이표체%반점잡교%TNF-α%IL-2%IL-6%IL-8
WORDS:PM2.5%WI-38 human embryo lung cell%differential expression of gene%dot blot hybridization%TNF-α%IL-2%IL-6%IL-8
目的：寻找与大气污染致病相关的相关基因,为阐明大气污染致病的生物学机制提供科学依据。方法采用mRNA 斑点杂交鉴定技术,克隆经采暖季≥75μg/m3 PM2.5与非采暖季<75μg/m3 PM2.5染毒的 WI-38人胚肺细胞,分析其间的基因表达差异。放免法测定炎性因子 TNF-α、IL-2、IL-6和 IL-8。结果与对照组比较,PM2.5>100μg/mL染毒24 h 后,WI-38人胚肺细胞细胞因子 TNF-α、IL-6和 IL-8明显升高,IL-2明显减低(P <0.05)。不同浓度 PM2.5处理的 WI-38人胚肺细胞间差异表达的基因片段,可见48份基因样本在350 bp 处出现清晰条带；该48份基因样本经斑点杂交后,Tester cDNA 杂交的48个斑点中,41份可见黑褐色斑点,而同样样本与 Driver cDNA 杂交的该48份样本均未见明显显色。结论PM2.5能诱导 WI-38人胚肺细胞产生炎性损伤,≥75μg/m3 PM2.5染毒的WI-38人胚肺细胞存在明显的基因损伤。
目的：尋找與大氣汙染緻病相關的相關基因,為闡明大氣汙染緻病的生物學機製提供科學依據。方法採用mRNA 斑點雜交鑒定技術,剋隆經採暖季≥75μg/m3 PM2.5與非採暖季<75μg/m3 PM2.5染毒的 WI-38人胚肺細胞,分析其間的基因錶達差異。放免法測定炎性因子 TNF-α、IL-2、IL-6和 IL-8。結果與對照組比較,PM2.5>100μg/mL染毒24 h 後,WI-38人胚肺細胞細胞因子 TNF-α、IL-6和 IL-8明顯升高,IL-2明顯減低(P <0.05)。不同濃度 PM2.5處理的 WI-38人胚肺細胞間差異錶達的基因片段,可見48份基因樣本在350 bp 處齣現清晰條帶；該48份基因樣本經斑點雜交後,Tester cDNA 雜交的48箇斑點中,41份可見黑褐色斑點,而同樣樣本與 Driver cDNA 雜交的該48份樣本均未見明顯顯色。結論PM2.5能誘導 WI-38人胚肺細胞產生炎性損傷,≥75μg/m3 PM2.5染毒的WI-38人胚肺細胞存在明顯的基因損傷。
목적：심조여대기오염치병상관적상관기인,위천명대기오염치병적생물학궤제제공과학의거。방법채용mRNA 반점잡교감정기술,극륭경채난계≥75μg/m3 PM2.5여비채난계<75μg/m3 PM2.5염독적 WI-38인배폐세포,분석기간적기인표체차이。방면법측정염성인자 TNF-α、IL-2、IL-6화 IL-8。결과여대조조비교,PM2.5>100μg/mL염독24 h 후,WI-38인배폐세포세포인자 TNF-α、IL-6화 IL-8명현승고,IL-2명현감저(P <0.05)。불동농도 PM2.5처리적 WI-38인배폐세포간차이표체적기인편단,가견48빈기인양본재350 bp 처출현청석조대；해48빈기인양본경반점잡교후,Tester cDNA 잡교적48개반점중,41빈가견흑갈색반점,이동양양본여 Driver cDNA 잡교적해48빈양본균미견명현현색。결론PM2.5능유도 WI-38인배폐세포산생염성손상,≥75μg/m3 PM2.5염독적WI-38인배폐세포존재명현적기인손상。
Objective To investigate the pathogen-related genes of atmospheric polluting disease so as to clarify the biology mechanism and provide the scientific basis.Methods By using the technique of dot blot hybridization,we analyzed genes’differential expression with cloning by exposure to ≥75 μg/m3 PM2.5 in heating season and < 75 μg/m3 PM2.5 in un-heating season in WI-38 human embryo lung cells.The levels of cytokines TNF-α,IL-2, IL-6 and IL-8 were determined by radio immunity assay. Results After 24h of treatment, compared with control group,more than 100μg/mL PM2.5 significantly increased TNF-α,IL-6 and IL-8 levels,and decreased IL-2 in WI-38 human embryo lung cells (P < 0.05 ).The clear stripe was found in 350 bp in 48 gene samples with segment with differential expression of genes exposed to different concentrations of PM2.5 in WI-38 human embryo lung cells.Through the dot blot hybridization,black brown spots were found in 41 samples in Tester cDNA hybridization,and no similar spots were found in all of the same samples in Driver cDNA hybridization. Conclusion PM2.5 exposure may induce the inflammatory damage of WI-38 human embryo lung cells.Obvious genetic damage was observed in those cells exposed to ≥75 μg/m3 PM2.5 in heating season.
