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西红花苷对三价砷致肝线粒体毒性的保护作用机制。

The mechanism of protective effect of crocin against liver mitochondrial toxicity caused by arsenic III.

机构信息

a Department of Pharmacodynamy and Toxicology, School of Pharmacy , Pharmaceutical Research Center, Mashhad University of Medical Sciences , Mashhad , Iran.

b Department of Pharmacology and Toxicology, Faculty of Pharmacy , Shahid Beheshti University of Medical Sciences , Tehran , Iran.

出版信息

Toxicol Mech Methods. 2018 Feb;28(2):105-114. doi: 10.1080/15376516.2017.1368054. Epub 2017 Aug 31.

DOI:10.1080/15376516.2017.1368054
PMID:28812436
Abstract

In this study, we want to understand whether crocin could prevent mitochondrial damage caused by As III. For this purpose, we determined different mitochondrial toxicity endpoints caused by As III. We evaluated mitochondrial ROS formation, lipid peroxidation, mitochondrial membrane potential (MMP) collapse, mitochondrial outer membrane integrity and cytochrome c release. Our results showed that pretreatment with crocin at a concentration of 25 µg/ml significantly (p < 0.001) reduced As III-induced mitochondrial ROS formation, lipid peroxidation, MMP collapse and mitochondrial swelling. Crocin also protected the mitochondria by decreasing the mitochondrial outer membrane damage that leads to reduce the amount of cytochrome c release. These results demonstrated that crocin is a promising antidotal candidate by ameliorating As III-induced oxidative stress through mitochondrial targeting.

摘要

在这项研究中,我们想了解藏红花苷是否可以预防 As III 引起的线粒体损伤。为此,我们确定了 As III 引起的不同线粒体毒性终点。我们评估了线粒体 ROS 的形成、脂质过氧化、线粒体膜电位(MMP)崩溃、线粒体外膜完整性和细胞色素 c 释放。我们的结果表明,用浓度为 25μg/ml 的藏红花苷预处理可显著(p<0.001)减少 As III 诱导的线粒体 ROS 的形成、脂质过氧化、MMP 崩溃和线粒体肿胀。藏红花苷还通过减少导致细胞色素 c 释放减少的线粒体外膜损伤来保护线粒体。这些结果表明,藏红花苷通过靶向线粒体减轻 As III 诱导的氧化应激,是一种有前途的解毒候选药物。

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