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作 者:柯珂[1] 朱燕[1] 曹毅[1] 杨光涛[1] 姜英[1] 吴凯[1] 杨旭[1]
机构地区:[1]华中师范大学生命科学学院环境科学实验室,武汉430079
出 处:《环境科学学报》2007年第7期1209-1213,共5页Acta Scientiae Circumstantiae
基 金:国家自然基金面上项目(No.30570799);湖北省科技攻关计划项目(No.2005AA307B01)~~
摘 要:为了验证吸入甲醛及气道氧化还原状态变化可在转录水平调控GSNOR表达,研究了甲醛环境暴露和抗氧化剂α-硫辛酸对小鼠肺中GSNOR表达的影响.以昆明系小鼠为实验材料,经吸入甲醛染毒和α-硫辛酸注射后立即脱颈处死,取其肺组织提取总RNA,采用RT-PCR二步法将其中GSNOR及管家基因β-actin扩增后,通过光密度分析染毒前后基因转录水平的变化.实验结果表明,与对照组相比,3.0mg·m-3浓度的甲醛可使GSNOR基因转录发生显著上调(p<0.01),而α-硫辛酸的注射可拮抗这种上调作用,表明吸入甲醛可在转录水平诱导GSNOR表达上调,而且这种上调与肺部的氧化还原状态改变有关,这可能是GSNOR在气道表达及其在哮喘发生中的作用基础.In order to test the hypothesis that formaldehyde and redox state in the airway could regulate GSNOR expression at the transcription level, effeets of environmental formaldehyde exposure and antioxidant α-lipoie aeid injeetion on GSNOR expression in miee lungs were investigated in the present study. Kunming purebred miee were used as experimental animals and the total RNA was extracted from the lungs immediately after exposure to formaldehyde and injection with α-lipoie acid. RT-PCR was applied to examine the transcriptional changes of GSNOR and β-aetin which was used as the eontrol gene. The results showed that eompared with eontrol groups, 3.0 mg· m^-3 formaldehyde exposure resulted in a signifieant inerease of GSNOR expression (p 〈 0.01 ), and α-lipoie acid injection completely blocked the increase. These results suggest that inhaled gaseous formaldehyde could induce up-regulation of GSNOR at the transeription level, and the ehanges may be related to an altered redox state in the lungs, whieh might provide a basis for the understanding of GSNOR expression in lungs.
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