高压氧暴露大鼠肺组织内PPAR通路分子变化规律

目的:研究高压氧暴露大鼠肺组织内过氧化物酶体增殖因子活化受体(PPAR)通路分子表达变化规律。方法:27只雄性SD大鼠随机分为高压常氧对照组(0.23 MPa空气)、高压氧时间序列处理组(0.23 MPa纯氧,分别暴露2 h、4 h、6 h和8 h),持续小流量通风,维持舱内O2浓度>99%。应用HE染色观察各组大鼠肺组织形态学变化;应用oligo芯片检测各个时间表达谱;应用RT-PCR验证发生改变的部分PPAR通路基因。结果:与高压常氧对照组相比,高压氧时间序列处理组造成的肺损伤逐渐加重;表达谱芯片的基因本体论(Go)富集分析结果中有一类PPAR通路类,包含有多个PPAR通路分子;RT-PCR结果提示PPARδ-和PPARγ-均在较长时间高压氧暴露的肺组织中上调。结论:高压氧长时间暴露造成的肺型氧中毒可引起PPAR通路的激活。

The variation of PPAR pathway molecules in the lung tissue of rats under hyperbaric oxygen exposure

Objective: To study the expression pattern of peroxisome proliferator-activated receptor(PPAR) pathway molecules in rat lung tissue under hyperbaric oxygen exposure.Methods: Twenty seven male SD rats were randomly divided into hyperbaric normoxia group(0.23 MPa air),hyperbaric oxygen treatment time series group(0.23 MPa oxygen,were exposed for 2 h,4 h,6 h or 8 h),continuous small flow of ventilation to maintain cabin O2 concentration >99%.HE staining of lung tissue morphological changes and application oligo microarray to each time point lung were observed.Part of the PPAR pathway genes were validated by RT-PCR.Results: Compared with hyperbaric normoxia group,the lung injury caused by hyperbaric oxygen treatment gradually deteriorated during the time series.Expression microarray analysis of gene ontology(Go) enrichment analysis results in a class of PPAR pathway class included multiple PPAR pathway molecule.RT-PCR results suggested that PPAR-δ and PPAR-γ were up-regulated in the lung tissue after a long time exposure to hyperbaric oxygen.Conclusion: Prolonged hyperbaric oxygen exposure causing pulmonary oxygen toxicity can induce the activation of the PPAR pathway.