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（+）-矢车菊素-3对大鼠脑脂质过氧化的影响。

Effect of (+)-cyanidanol-3 on rat brain lipid peroxidation.

作者信息

Fehér J, Blázovics A, Cornides A, Vereckei A

出版信息

Br J Exp Pathol. 1985 Apr;66(2):161-4.

PMID:3986129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2041046/
Abstract

Non-enzymic lipid peroxidation was stimulated in homogenates, plasma membrane fractions and microsomes of rat brain in vitro by incubation with ascorbic acid. Malondialdehyde formation was determined by the thiobarbituric acid test. It has been established that (+)-cyanidanol-3 inhibits the ascorbic acid-stimulated lipid peroxidation in various fractions of rat brain. On the basis of these results it is suggested that (+)-cyanidanol-3 treatment protects brain suspensions against lipid peroxidation by acting as a free radical scavenger in vitro.

摘要

通过与抗坏血酸一起孵育，在体外刺激大鼠脑匀浆、质膜组分和微粒体中的非酶脂质过氧化。通过硫代巴比妥酸试验测定丙二醛的形成。已经确定，（+）-花青素-3抑制抗坏血酸刺激的大鼠脑各组分中的脂质过氧化。基于这些结果，表明（+）-花青素-3处理通过在体外作为自由基清除剂来保护脑悬液免受脂质过氧化。

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本文引用的文献

1
Protective effect of (+)cyanidanol-3 in acute liver injury induced by galactosamine or carbon tetrachloride in the rat.（+）-矢车菊素-3对大鼠半乳糖胺或四氯化碳诱导的急性肝损伤的保护作用。
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Reduced triphosphopyridine nucleotide oxidase-catalyzed alterations of membrane phospholipids. VI. Structural changes in mitochondria associated with inactivation of electron transport activity.
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Lipid peroxidation as the cause of the ascorbic acid induced decrease of adenosine triphosphatase activities of rat brain microsomes and its inhibition by biogenic amines and psychotropic drugs.
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