核黄素
肺
外渗
药理学
髓过氧化物酶
医学
缺血
脂质过氧化
维生素
血管通透性
埃文斯蓝
维生素E
化学
麻醉
免疫学
内科学
炎症
氧化应激
抗氧化剂
生物化学
作者
Andreas Seekamp,Donald E. Hultquist,Gerd O. Till
出处
期刊:Inflammation
[Springer Nature]
日期:1999-01-01
卷期号:23 (5): 449-460
被引量:51
标识
DOI:10.1023/a:1021965026580
摘要
The effect of vitamin B2 (riboflavin) on oxidant-mediated acute lung injury has been examined in three different rat models. Pulmonary injury was induced by intravenous injection of cobra venom factor (CVF), by the intrapulmonary deposition of IgG immune complexes, or by hind limb ischemia-reperfusion. In each of the three models, injury was characterized by increases in vascular permeability (leakage of 125I-labeled bovine serum albumin), alveolar hemorrhage (extravasation of 51Cr-labeled rat erythrocytes), and neutrophil accumulation (myeloperoxidase activity). Intraperitoneal administration of riboflavin at a dose of 6 micromoles/kg body weight reduced vascular leakage by 56% in the CVF model, by 31% in the immune complex model, and by 53% in the lung injury model following ischemia-reperfusion of the hind limbs. Similar treatment reduced hemorrhage by 76%, 51%, and 70% in the three models of lung injury. In the CVF model, riboflavin was also shown to decrease products of lipid peroxidation (conjugated dienes) in lungs (by 45%) and in plasma (by 74%). Neutrophil accumulation in the lungs was not influenced by riboflavin administration in any of the three models. The studies demonstrate that riboflavin can mount a significant protection against oxidant-mediated inflammatory organ injury.
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