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OXIDATIVE STRESS IN GSNO REDUCTASE REGULATION IN MICE LUNGS

机译:氧化应激对小鼠腰果GSno还原酶的调节作用

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摘要

In order to explore the molecular regulation of GSNO reductase (GSNOR), effects of environmental formaldehyde exposure and antioxidant -lipoic acid (LA) injection on GSNOR activity and expression in mice lungs were investigated in the present study. Results showed that GSNOR activity was elevated upon 3.0 mg/m3 FA exposure (compared with 0 mg/m3 FA inhaled group, p<0.01) and the elevation was completely inhibited by LA injection (compared with 3.0 mg/m3 FA inhaled group, p<0.01). Meanwhile, GSH levels were significantly decreased in 3.0 mg/m3 FA inhaled group (compared with 0 mg/m3 FA inhaled group, p<0.01), and were regenerated by LA injection (compared with 3.0 mg/m3 FA inhaled group, p<0.01). The expression of GSNOR by using RT-PCR method correlated with the results of GSNOR activity assay. The results indicated that gaseous FA might activate GSNOR, and the activation may be related with the increase of oxidative stress. Since GSNOR has a central role in mediating SNO signaling and asthma development, these findings also suggested that indoor air pollutants such as FA might be key risk factors for the rise in asthma cases.
机译:为了探索GSNO还原酶(GSNOR)的分子调控,本研究研究了环境甲醛暴露和抗氧化剂-硫辛酸(LA)注射对小鼠肺中GSNOR活性和表达的影响。结果表明,在暴露于3.0 mg / m3 FA的情况下,GSNOR活性升高(与0 mg / m3 FA吸入的组相比,p <0.01),并且通过LA注射完全抑制了其升高(与吸入3.0 mg / m3 FA的组相比,p <0.01)。同时,3.0 mg / m3 FA吸入组的GSH水平显着降低(与0 mg / m3 FA吸入组相比,p <0.01),并通过LA注射再生(与3.0 mg / m3 FA FA吸入组相比,p <0.01)。 0.01)。 RT-PCR法检测GSNOR的表达与GSNOR活性测定结果有关。结果表明,气态FA可能激活GSNOR,且激活可能与氧化应激的增加有关。由于GSNOR在介导SNO信号和哮喘发展中起着核心作用,因此这些发现还表明,室内空气污染物(例如FA)可能是哮喘病例上升的关键危险因素。

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