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目的观察不同复氧方式对慢性缺氧幼年大鼠肺组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-10(IL-10)mRNA的表达的影响。方法5周龄雄性SD大鼠54只,随机均分为三组Ⅰ和Ⅱ组大鼠分别在常压低氧(FiO2=10%)下持续缺氧2周后快速纯氧或21%O2复氧3h;Ⅲ组大鼠行间断缺氧(慢性缺氧同Ⅰ组,但每天暴露于空气中1h)2周后快速纯氧复氧3h。各组大鼠分别于复氧后0、1、3h留取肺组织标本。逆转录-聚合酶链反应(RT-PCR)方法检测肺组织TNF-α、IL-1β、IL-10mRNA表达水平,光镜下观察肺组织病理改变。结果与复氧前相比,Ⅰ组大鼠肺组织TNF-α、IL-1βmRNA在复氧1、3h明显升高(P<0.01),IL-10mRNA表达在复氧3h后明显升高(P<0.01)。Ⅱ、Ⅲ组大鼠肺组织复氧1、3hTNF-α、IL-1βmRNA的表达和复氧3hIL-10mRNA表达均明显低于Ⅰ组(P<0.01)。肺组织病理检查见Ⅱ、Ⅲ组大鼠的肺损伤均较Ⅰ组明显减轻。结论慢性缺氧幼鼠肺组织复氧损伤早期存在炎症介质/抗炎介质失衡,21%O2复氧及复氧前间断吸入21%O2可明显减少复氧后炎性因子的表达和减轻复氧引起的肺损伤。
Objective To observe the effects of different reoxygenation on the expression of TNF-α, IL-1β and IL-10 in lung tissue of chronic hypoxic rats Impact. Methods Fifty-four male Sprague-Dawley rats were randomly divided into three groups. Rats in groups I and II were treated with rapid oxygen or 21% O2 after 2 weeks of hypoxia (FiO2 = 10% Oxygen for 3 hours. Rats in group Ⅲ were subjected to rapid oxygen reoxygenation 3 hours after intermittent hypoxia (chronic hypoxia and group Ⅰ, but exposed to the air for 1 hour every day). The rats in each group were taken lung samples at 0,1,3 h after reoxygenation. The expression of TNF-α, IL-1β and IL-10 mRNA in lung tissue were detected by reverse transcription-polymerase chain reaction (RT-PCR) Results Compared with the pre-reoxygenation group, the levels of TNF-α and IL-1βmRNA in lung tissue of rats in group Ⅰ were significantly increased at 1 h and 3 h after reoxygenation (P <0.01), while the expression of IL-10 mRNA increased significantly <0.01). The mRNA expression of 1,3 hTNF-α, IL-1β in reoxygenation group and 3h IL-10 mRNA expression in reoxygenation group were significantly lower than those in group Ⅰ (P <0.01). Pathological examination of lung tissue in group Ⅱ, Ⅲ showed lung injury were significantly reduced compared with group Ⅰ. Conclusions There is imbalance of inflammatory mediators / antiinflammatory mediators in early stage of reoxygenation injury in young rats with chronic hypoxia. 21% O2 reoxygenation and intermittent inhalation of 21% O2 before reoxygenation significantly reduce the expression of inflammatory cytokines and reoxygenation Induced lung injury.