| 薛盼盼,刘远凤,姜小军,封少龙.大蒜素改善PM2.5致HUVEC氧化应激和凋亡.[J].中南医学科学杂志.,2022,(5):632-636. |
| 大蒜素改善PM2.5致HUVEC氧化应激和凋亡 |
| Mechanism of Allicin in improving oxidative stress and apoptosis of HUVEC induced by PM2.5 |
| 投稿时间：2022-03-15 修订日期：2022-05-02 |
| DOI：10.15972/j.cnki.43-1509/r.2022.05.003 |
| 中文关键词: 大蒜素 PM2.5 人脐静脉内皮细胞 氧化应激 凋亡 [ |
| 英文关键词:Allicin PM2.5 HUVEC oxidative stress apoptosis |
| 基金项目:国家自然科学基金(41877390)；有机地球化学国家重点实验室开放课题(SKLOG202010) 作者简介:薛盼盼,硕士研究生,研究方向为大气细颗粒物影响心血管健康的细胞与分子机制,E-mail为3132904790@qq.com。通信作者封少龙,博士,教授,硕士研究生导师,研究方向为毒害污染物的环境行为及其影响人体健康的细胞与分子机制,E-mail为slfeng@glmc.edu.cn。 |
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| 中文摘要: |
| 目的研究大蒜素改善细颗粒物(PM2.5)诱导的人脐静脉内皮细胞(HUVEC)氧化应激和凋亡的机制。 方法细胞分为对照组、PM2.5组、大蒜素组和大蒜素联合组。CCK8法、抗氧化酶相关试剂盒、JC-1荧光探针法、流式细胞术、qRT-PCR和Western blotting法测定细胞活力、凋亡率、氧化应激、线粒体损伤、氧化应激和凋亡途径相关基因的mRNA和蛋白质的表达。 结果与PM2.5组比较,大蒜素联合组细胞活力增高,氧化应激反应减弱,细胞凋亡降低。大蒜素能够阻断细胞内凋亡途径的信号转导,激活Kelch样环氧氯丙胺相关蛋白1(Keap-1)/核转录因子E2相关因子2(Nrf2)通路,促进大蒜素联合组中抗氧化酶的表达。 结论大蒜素通过激活Keap-1/Nrf2通路保护HUVEC免受PM2.5介导的氧化应激和细胞凋亡的损害。 |
| 英文摘要: |
| To investigate the molecular mechanism of Allicin protecting human umbilical vein endothelial cells (HUVEC) from particulate matter 2.5 (PM2.5)-induced oxidative stress and apoptosis. MethodsThe cell experiment was divided into four groups:control group, PM2.5 group, Allicin group and Allicin-combined group. CCK8 assay, antioxidant oxidase-related kit, JC-1 fluorescence probe, flow cytometry, qRT-PCR and Western blotting were used to determine cell viability, apoptosis rate, oxidative stress, mitochondrial damage, oxidative stress and apoptosis pathway related genes mRNA and protein expression. ResultsCompared with the PM2.5 group, the Allicin combined group increased cell viability, decreased oxidative stress response and cell apoptosis. Allicin was able to block the signal transduction of the intracellular apoptosis and activate the Keap-1/nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway, and promote the expression of antioxidative enzymes in the Allicin combined group. ConclusionAllicin protects HUVEC from PM2.5 mediated oxidative stress and apoptosis mediated by activating the Keap-1/Nrf2 pathway. |
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