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巴西绿蜂胶部分通过PI3K/Akt/mTOR介导的Nrf2/HO-1途径抑制人脐静脉内皮细胞中氧化低密度脂蛋白诱导的氧化应激。

Brazilian Green Propolis Inhibits Ox-LDL-Stimulated Oxidative Stress in Human Umbilical Vein Endothelial Cells Partly through PI3K/Akt/mTOR-Mediated Nrf2/HO-1 Pathway.

作者信息

Yuan Wenwen, Chang Huasong, Liu Xinying, Wang Shiqiang, Liu Hui, Xuan Hongzhuan

机构信息

School of Life Science, Liaocheng University, Liaocheng 252059, China.

Center of Bee Industry on Seed-Breeding and Popularization in Shandong Province, Tai'an, China.

出版信息

Evid Based Complement Alternat Med. 2019 Jul 7;2019:5789574. doi: 10.1155/2019/5789574. eCollection 2019.

DOI:10.1155/2019/5789574
PMID:31360208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6642762/
Abstract

Propolis has been widely used as a dietary supplement for its health benefits, including cardiovascular protective effects. The aim of this study was to investigate the cytoprotective effects of Brazilian green propolis (BP) against oxidized low-density lipoprotein (Ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage. Our results suggested that treatment with BP rescued Ox-LDL-stimulated HUVECs cell viability losses, which might be associated with its inhibitive effects on the cell apoptosis and autophagy. We also noticed that BP restored Ox-LDL-stimulated HUVECs oxidative stress, by induced antioxidant gene expressions, including Heme oxygenase-1 and its upstream mediator, Nrf2, which were mediated by the activation of the phosphorylation of PI3K/Akt/mTOR. Pretreatment with wortmannin, PI3K/AKT inhibitor, abolished BP induced Nrf2 nuclear translocation and HO-1 level. Our results demonstrated that BP protected HUVECs against oxidative damage partly via PI3K/Akt/mTOR-mediated Nrf/HO-1 pathway, which might be applied into preventing Ox-LDL mediated cardiovascular diseases.

摘要

蜂胶因其对健康有益,包括对心血管的保护作用,而被广泛用作膳食补充剂。本研究的目的是探讨巴西绿蜂胶(BP)对氧化低密度脂蛋白(Ox-LDL)诱导的人脐静脉内皮细胞(HUVECs)损伤的细胞保护作用。我们的结果表明,BP处理可挽救Ox-LDL刺激的HUVECs细胞活力损失,这可能与其对细胞凋亡和自噬的抑制作用有关。我们还注意到,BP通过诱导抗氧化基因表达,包括血红素加氧酶-1及其上游介质Nrf2,恢复了Ox-LDL刺激的HUVECs氧化应激,这是由PI3K/Akt/mTOR磷酸化的激活介导的。用渥曼青霉素(PI3K/AKT抑制剂)预处理可消除BP诱导的Nrf2核转位和HO-1水平。我们的结果表明,BP部分通过PI3K/Akt/mTOR介导的Nrf/HO-1途径保护HUVECs免受氧化损伤,这可能应用于预防Ox-LDL介导的心血管疾病。

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