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[脂质体包裹的重组人超氧化物歧化酶(脂质体-r-h-SOD)对豚鼠福斯曼抗血清诱导的肺损伤的影响]

[Effect of liposome-encapsulated recombinant human superoxide dismutase (liposome-r-h-SOD) on the lung injury induced by Forssman antiserum in guinea pigs].

作者信息

Nakagami K, Inamura M, Nakano Y, Kobayashi Y

机构信息

Medicinal Research Laboratory, Toyo Jozo Co., Ltd., Shizuoka, Japan.

出版信息

Nihon Yakurigaku Zasshi. 1991 Jan;97(1):41-9. doi: 10.1254/fpj.97.1_41.

Abstract

We investigated the effect of liposome-r-h-SOD on the lung injury induced by Forssman antiserum in guinea pigs. Intravenous injection of Forssman antiserum produced a biphasic increase in pulmonary resistance in guinea pigs. Liposome-r-h-SOD blocked this biphasic increase in a dose-dependent manner. Exudate and hemorrhage in the alveolar spaces and connective tissues were blocked by liposome-r-h-SOD. Liposome-r-h-SOD was more effective when it was injected 30 min prior to challenge than 5 min prior to challenge. On the other hand, free r-h-SOD or a mixture of free r-h-SOD and empty liposome did not block the lung injury. SOD activity in porcine endothelial cells cultured with liposome-r-h-SOD increased in a dose-dependent and time-dependent manner, while it did not increase with free r-h-SOD. Exogenous SOD was detected by immunoperoxidase staining in endothelial cells of arterioles and capillaries and in alveolar epithelial cells of the lung of guinea pigs injected with liposome-r-h-SOD. These findings suggest that superoxide radical may take part in the lung injury induced by Forssman antiserum. Liposome-r-h-SOD, which adheres to and/or is endocytosed by endothelial cells, may protect the lung from oxygen radicals.

摘要

我们研究了脂质体重组人超氧化物歧化酶(liposome-r-h-SOD)对豚鼠福斯曼抗血清诱导的肺损伤的影响。静脉注射福斯曼抗血清可使豚鼠肺阻力呈双相性增加。脂质体-r-h-SOD以剂量依赖的方式阻断了这种双相性增加。脂质体-r-h-SOD可阻断肺泡腔和结缔组织中的渗出液和出血。在攻击前30分钟注射脂质体-r-h-SOD比在攻击前5分钟注射更有效。另一方面,游离的重组人超氧化物歧化酶(r-h-SOD)或游离r-h-SOD与空脂质体的混合物不能阻断肺损伤。用脂质体-r-h-SOD培养的猪内皮细胞中的超氧化物歧化酶(SOD)活性呈剂量和时间依赖性增加,而游离r-h-SOD则不会使其增加。在注射了脂质体-r-h-SOD的豚鼠的肺小动脉和毛细血管内皮细胞以及肺泡上皮细胞中,通过免疫过氧化物酶染色检测到了外源性SOD。这些发现表明,超氧阴离子可能参与了福斯曼抗血清诱导的肺损伤。附着于内皮细胞和/或被内皮细胞内吞的脂质体-r-h-SOD可能保护肺免受氧自由基的损伤。

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