烟雾吸入性肺损伤肺泡表面活性物质结合蛋白A表达异常机制的研究

STUDY ON THE MECHANISMS OF ABNORMAL SPA EXPRESSION AFTER SMOKE INHALATION INJURY

为探讨烟雾吸入性肺损伤肺泡表面活性物质结合蛋白A (SPA)表达异常机制。本实验采用烟雾吸入性肺损伤大鼠模型 ,研究吸入伤后肺氧化应激及SPAmRNA表达情况。提取SPA转录因子(TTF1) ,采用EMSA实验 ,研究氧化应激对TTF1与SPA基因调控区DNA结合活性的影响。结果发现 ,烟雾吸入伤后肺组织过氧化氢 (H2 O2 )含量显著增加 ,SPAmRNA表达下降 ;EMSA实验显示 ,H2 O2 剂量依赖地抑制TTF1与SPA基因调控区DNA结合活性。研究表明 ,氧化应激对TTF1活性抑制可能是烟雾吸入性肺损伤SPA表达下降的原因。

The aim of this study was to investigate the mechanism of abnormal SPA expression after smoke inhalation injury (SII).The rat model with SII was used to observe the expression of SPA and the level of H 2 O 2 in the lung tissue. EMSA was performed to study the effect of H 2 O 2 on the TTF 1 binding activity in regulating area of SPA gene. The results showed that H 2 O 2 was increased, and the expression of SPA was down regulated in lung tissue after smoke inhalation injury. H 2 O 2 could inhibit the TTF 1 binding activity in SPA regulating area in vitro . Our results suggested that the inhibition of TTF 1 activity by oxidative stress might be the mechanism of abnormal SPA expression after SII.