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百里醌对大鼠甲醛诱导的神经毒性的保护作用。

Protection with thymoquinone against formaldehyde-induced neurotoxicity in the rats.

作者信息

Saygin B, Esrefoglu M, Bayindir N, Tok O E, Selek S, Bulut H, Ozer O F, Ozturk A, Yilmaz O, Meydan S

出版信息

Bratisl Lek Listy. 2018;119(11):726-730. doi: 10.4149/BLL_2018_129.

DOI:10.4149/BLL_2018_129
PMID:30686007
Abstract

INTRODUCTION

This study aimed to investigate the neurotoxic damage of formaldehyde (FA), which is commonly used in medicine and industrial fields, for the hippocampus of rats and the protective role of thymoquinone (TQ) against this neurotoxicity.

METHODS

There were five groups with eight rats in each. Two control groups were formed, in one of them physiological saline was applied and in the other one corn oil was applied. FA was injected in Group 3. Group 4 was exposed to FA and TQ simultaneously. Group 5 received TQ only. At the end of the experiment animals were sacrificed and brain tissues were removed for biochemical and histopathological investigation.

RESULTS

catalase (CAT), glutathione peroxidase (GSH-px) and superoxide dismutase (SOD), all known as enzymes with antioxidant activities, were increased in FA and TQ simultaneously administered group. FA caused prominent subarachnoidal hemorrhage and vacuolization. Vacuolization was not observed but occasional subarachnoidal hemorrhage was detected in the FA+TQ group.

CONCLUSION

Neurotoxic damage in hippocampus induced by FA was reverted by administration of TQ (Tab. 1, Fig. 1, Ref. 26).

摘要

引言

本研究旨在探讨医学和工业领域常用的甲醛(FA)对大鼠海马体的神经毒性损伤以及黑种草醌(TQ)对这种神经毒性的保护作用。

方法

共分五组,每组八只大鼠。设立两个对照组,一组给予生理盐水,另一组给予玉米油。第三组注射FA。第四组同时暴露于FA和TQ。第五组仅接受TQ。实验结束时处死动物,取出脑组织进行生化和组织病理学检查。

结果

同时给予FA和TQ的组中,过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-px)和超氧化物歧化酶(SOD)这三种已知具有抗氧化活性的酶均有所增加。FA导致明显的蛛网膜下腔出血和空泡化。在FA+TQ组未观察到空泡化,但偶尔检测到蛛网膜下腔出血。

结论

给予TQ可逆转FA诱导的海马体神经毒性损伤(表1,图1,参考文献26)。

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