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脂多糖处理的红细胞中羟基自由基的产生及膜流动性

Hydroxyl radical generation and membrane fluidity of erythrocytes treated with lipopolysaccharide.

作者信息

Hino Y, Kumashiro R, Sata M, Nishi J, Ogura R, Tanikawa K

机构信息

Second Department of Medicine, Kurume University School of Medicine, Japan.

出版信息

Free Radic Res Commun. 1993;19 Suppl 1:S177-84. doi: 10.3109/10715769309056s177.

Abstract

The effect of lipopolysaccharide (LPS) and/or bile acids on rat erythrocyte membranes was studied in vitro. Addition of LPS isolated from E. coli (J5 mutant) into the erythrocyte resulted in the decrease of membrane fluidity as determined by spin labelling using electron paramagnetic resonance (EPR). This was accompanied by membrane fragility. It was found that hydroxyl radicals were generated from erythrocytes treated with LPS by using DMPO spin trapping. However, pretreatment of erythrocytes with taurine-conjugated bile acids was found to modify the membrane response induced by LPS. Taurocholic acid (TCA) and tauroursodeoxycholic acid (TUDCA) prevented the decrease of membrane fluidity induced by LPS, and, as a result, the membrane integrity was maintained although no significant changes were observed in the amount of hydroxyl radicals produced by LPS addition. However, taurochenodeoxycholic acid (TCDCA) exhibited little beneficial effect on the dynamic properties and the function of the erythrocyte membranes, although the hydroxyl radical declined markedly in the erythrocytes. Therefore, it is suggested that TCA and TUDCA have a protective effect against LPS-induced membrane fragility by modulating membrane fluidity.

摘要

在体外研究了脂多糖(LPS)和/或胆汁酸对大鼠红细胞膜的影响。将从大肠杆菌(J5突变体)分离的LPS添加到红细胞中,通过电子顺磁共振(EPR)自旋标记测定,结果导致膜流动性降低。这伴随着膜脆性增加。通过使用DMPO自旋捕获发现,用LPS处理的红细胞会产生羟基自由基。然而,发现用牛磺酸结合的胆汁酸预处理红细胞可改变LPS诱导的膜反应。牛磺胆酸(TCA)和牛磺熊去氧胆酸(TUDCA)可防止LPS诱导的膜流动性降低,结果,尽管添加LPS产生的羟基自由基数量没有明显变化,但膜完整性得以维持。然而,牛磺鹅去氧胆酸(TCDCA)对红细胞膜的动态特性和功能几乎没有有益影响,尽管红细胞中的羟基自由基明显减少。因此,提示TCA和TUDCA通过调节膜流动性对LPS诱导的膜脆性具有保护作用。

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