230kPa纯氧暴露不同时程小鼠肺组织TLR4基因表达的变化

Expression of TLR4 gene in mice exposed to 230 kPa hyperbaric oxygen during different time courses

目的观察TLR4基因在肺型氧中毒中的表达情况，探讨TLR4在肺型氧中毒发病过程中的作用。方法将40只小鼠随机分为对照组（肺型氧中毒剂量单位UPTD=0），230kPa（绝对压）纯氧暴露2h组（UPTD=347）、6h组（UPTD=1044）、10h组（UPTD=1740），和常氧高氮组（UPTD=0）。分别进行病理学观察，检测肺湿／干质量比和肺组织TLR4基因表达情况。结果随着暴露时间的延长，肺组织损伤严重程度逐渐加深，肺湿／干质量比值逐渐增加，TLR4表达逐渐降低，TLR4表达量与UPTD呈负相关（r=0．956，P〈0．01）。结论TLR4可能参与了肺型氧中毒的发病过程，其机制有待进一步研究。

Objective To investigate the expression of TLR4 gene in mice exposed to 230 kPa hyperbaric oxygen during different time courses, and the role of TLR4 in the development of pulmonary oxygen toxicity. Methods Forty C57BL/6 mice were randomly divided into 4 groups： the control group（ UPTD, unit pulmonary toxicity dose = 0） , the 2-h exposure to 230 kPa oxygen group （ UPTD = 347）, the 6-h group （ UPTD = 1044） , the 10-h group （UPTD -- 1740） , the norm oxygen group （hyperbaric and normal 02 density group）. Pathologic changes in the pulmonary tissue were observed and weight ratio of wet lung to dry lung and the expression of TLR4 were measured in vivo by using applied quantitative real time PCR. Results Puhnonary collapse hemorrhage, congestion and leucocyte aggregation in lung interstitium were observed in mice exposed to pure oxygen. Conclusions Lesion of the pulmonary tissue in mice deteriorated gradually with the extension of exposure. Highly negative correlation between TLR4 and UPTD indicated that TLR4 might be involved in the development of pulmonary oxygen toxicity, whose mechanism remained to be explored.