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血小板活化因子受体拮抗剂BN 52021可改善实验性出血性休克所致肺脏抗氧化防御系统的减弱。

BN 52021, PAF-receptor antagonist, improves diminished antioxidant defense system of lungs in experimentally induced haemorrhagic shock.

作者信息

Makarewicz-Płońska M, Witek A, Farbiszewski R

机构信息

Department of Analytical Chemistry, Medical University, Białystok, Poland.

出版信息

Pol J Pharmacol. 1998 May-Jun;50(3):265-9.

PMID:9861635
Abstract

The purpose of our experiments was to determine whether BN 52021, PAF-receptor antagonist, has any influence on the production of reactive oxygen species in the lung induced by haemorrhagic shock. The results showed, that the activities of Cu,Zn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the lung after haemorrhagic shock were decreased in comparison with control and sham groups while the activity of glutathione reductase (GSSG-R) was unchanged. The content of SH-groups was decreased while thiobarbituric acid reacting substances (TBA-rs) after haemorrhagic shock were increased. Infusion of BN 52021 (5.0 mg/kg i.v.) in haemorrhagic animals caused significantly increased activities of Cu,Zn-SOD, GSH-Px, GSSG-R in the lung. The SH-group level was slightly increased while TBA-rs returned to normal values.

摘要

我们实验的目的是确定血小板活化因子受体拮抗剂BN 52021是否对失血性休克诱导的肺中活性氧的产生有任何影响。结果显示,与对照组和假手术组相比,失血性休克后肺中铜锌超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性降低,而谷胱甘肽还原酶(GSSG-R)的活性未改变。巯基含量降低,而失血性休克后硫代巴比妥酸反应物质(TBA-rs)增加。对失血性动物静脉注射BN 52021(5.0毫克/千克)可使肺中铜锌SOD、GSH-Px、GSSG-R的活性显著增加。巯基水平略有升高,而TBA-rs恢复到正常水平。

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BN 52021, PAF-receptor antagonist, improves diminished antioxidant defense system of lungs in experimentally induced haemorrhagic shock.血小板活化因子受体拮抗剂BN 52021可改善实验性出血性休克所致肺脏抗氧化防御系统的减弱。
Pol J Pharmacol. 1998 May-Jun;50(3):265-9.
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Platelet-activating factor receptor-antagonist (BN 52021) stabilizes the oxidative-antioxidative balance and attenuates the morphological changes in the gastrointestinal tract in experimental hemorrhagic shock.血小板活化因子受体拮抗剂(BN 52021)可稳定氧化-抗氧化平衡,并减轻实验性失血性休克时胃肠道的形态学改变。
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