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白藜芦醇对一氧化碳诱导的雄性大鼠毒性的神经保护作用

Neuro-Protective Effects of Resveratrol on Carbon Monoxide-Induced Toxicity in Male Rats.

作者信息

Tabrizian Kaveh, Shahraki Jafar, Bazzi Mohadeseh, Rezaee Ramin, Jahantigh Hosseinali, Hashemzaei Mahmoud

机构信息

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Zabol University of Medical Sciences, Zabol, Iran.

Students Research Committee, School of Pharmacy, Zabol University of Medical Sciences, Zabol, Iran.

出版信息

Phytother Res. 2017 Sep;31(9):1310-1315. doi: 10.1002/ptr.5855. Epub 2017 Jun 21.

Abstract

Acute carbon monoxide (CO) poisoning causes neurotoxicity through induction of necrosis, apoptosis, lipid peroxidation and oxidative stress. Resveratrol (RES) is a natural polyphenolic phytoalexin that exhibits neuroprotective effects in ischemia/reperfusion due to its anti-apoptotic, anti-necrotic and strong anti-oxidant properties as well as its ability to activate pro-survival pathways. In this study, rats were exposed to CO 3000 ppm for 1 h. Immediately after poisoning and on the next four consecutive days, RES (1, 5 and 10 mg/kg) was administered intraperitoneally. On the fifth day, animals' brains were excised, and necrosis, lipid peroxidation level and the level of Akt, BAX and BCL2 expression were evaluated. The results showed that RES 10 mg/kg significantly reduced lipid peroxidation, but RES 1 and 5 mg/kg had no significant effect on this parameter. Furthermore, RES 5 and 10 mg/kg significantly increased Akt expression level, while BAX/BCL2 ratio was reduced by RES 1, 5 and 10 mg/kg. Moreover, RES reduced necrotic foci in the brain, but the best results were seen following treatment with RES 10 mg/kg. In summary, RES showed neuroprotective effect in CO-poisoned rats as it decreased necrosis and BAX/BCL2 ratio and increased Akt expression levels. Copyright © 2017 John Wiley & Sons, Ltd.

摘要

急性一氧化碳(CO)中毒通过诱导坏死、凋亡、脂质过氧化和氧化应激导致神经毒性。白藜芦醇(RES)是一种天然多酚类植物抗毒素,由于其具有抗凋亡、抗坏死和强大的抗氧化特性以及激活促生存途径的能力,在缺血/再灌注中表现出神经保护作用。在本研究中,将大鼠暴露于3000 ppm的CO中1小时。中毒后立即以及在接下来连续四天,腹腔注射RES(1、5和10 mg/kg)。在第五天,切除动物的大脑,评估坏死、脂质过氧化水平以及Akt、BAX和BCL2的表达水平。结果表明,10 mg/kg的RES显著降低脂质过氧化,但1和5 mg/kg的RES对该参数无显著影响。此外,5和10 mg/kg的RES显著增加Akt表达水平,而1、5和10 mg/kg的RES降低BAX/BCL2比值。此外,RES减少了大脑中的坏死灶,但10 mg/kg的RES治疗后效果最佳。总之,RES在CO中毒大鼠中显示出神经保护作用,因为它降低了坏死和BAX/BCL2比值,并增加了Akt表达水平。版权所有© 2017约翰威立父子有限公司。

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