Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury
Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury
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DOI：
10.1152/ajplung.00191.2002
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发表时间：
2003-04-01
影响因子：
4.9
通讯作者：
Crapo, JD
中科院分区：
文献类型：
--
作者：
Bowler, RP;Arcaroli, J;Crapo, JD
出血导致超氧化物的过度产生，这与严重的肺损伤有关。我们研究了超氧化物歧化酶（SOD）模拟锰（III）mesotetrakis（di-N-乙基咪唑）卟啉（AEOL 10150）是否可以减轻这种肺损伤，以及细胞外（EC）-SOD缺陷小鼠是否会增加肺损伤诱导的肺损伤。与野生型小鼠相比，EC-SOD缺陷小鼠在出血后1 h肺中性粒细胞蓄积增加，髓过氧化物酶活性增加3.9倍，核因子（NF）-kappaB活化增加1.5倍，脂质过氧化增加1.5倍。用AEOL 10150预处理未减弱中性粒细胞蓄积，但显著降低了野生型和EC-SOD缺陷小鼠的NF-κ B活化和脂质过氧化。EC-SOD缺陷小鼠肺内中性粒细胞聚集的增加表明EC-SOD可能在介导中性粒细胞向肺的募集中起作用。
Hemorrhage results in excessive production of superoxide that is associated with severe lung injury. We examined whether the superoxide dismutase (SOD) mimetic manganese( III) mesotetrakis (di-N-ethylimidazole) porphyrin (AEOL 10150) could attenuate this lung injury and whether extracellular (EC)-SOD-deficient mice would have increased hemorrhage-induced lung injury. Compared with wild-type mice, EC-SOD-deficient mice had increased lung neutrophil accumulation, a 3.9-fold increase in myeloperoxidase activity, a 1.5-fold increase in nuclear factor (NF)-kappaB activation, and a 1.5-fold increase in lipid peroxidation 1 h after hemorrhage. Pretreatment with AEOL 10150 did not attenuate neutrophil accumulation but significantly reduced NF-kappaB activation and lipid peroxidation in both wild-type and EC-SOD-deficient mice. The increase in hemorrhage-induced neutrophil accumulation in the lungs of EC-SOD-deficient mice suggests that EC-SOD might play a role in mediating neutrophil recruitment to the lung.