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原儿茶酸通过激活依赖腺苷一磷酸激活蛋白激酶的途径改善内皮细胞中棕榈酸诱导的氧化损伤。

Protocatechuic Acid Ameliorated Palmitic-Acid-Induced Oxidative Damage in Endothelial Cells through Activating Endogenous Antioxidant Enzymes via an Adenosine-Monophosphate-Activated-Protein-Kinase-Dependent Pathway.

机构信息

The Chongqing Engineering Laboratory for Green Cultivation and Deep Processing of the Three Gorges Reservoir Area's Medicinal Herbs, College of Biology and Food Engineering , Chongqing Three Gorges University , Chongqing 404100 , People's Republic of China.

出版信息

J Agric Food Chem. 2018 Oct 10;66(40):10400-10409. doi: 10.1021/acs.jafc.8b03414. Epub 2018 Sep 26.

DOI:10.1021/acs.jafc.8b03414
PMID:30220205
Abstract

Protocatechuic acid (PCA, 3,4-dihydroxybenzoic acid), the main metabolite of anthocyanins, is widely distributed in fruits and vegetables and has been reported to possess a strong antioxidant activity. Herein, we aimed to investigate the protective effect of PCA against high palmitic-acid (PA)-induced oxidative damage and the underling molecular mechanisms in human umbilical vein endothelial cells (HUVECs). PCA reduced the levels of intracellular reactive oxygen species and malondialdehyde and increased the activities of endogenous antioxidant enzymes, including superoxide dismutase, glutathione peroxidase 1, and heme oxygenase 1 (HO-1). Metabolomic analysis showed that PCA affected numerous metabolites, especially some of which were related with energy metabolism. PCA also upregulated the phosphorylation of adenosine-monophosphate-activated protein kinase (AMPK) at Thr through activating liver kinase B1 and then promoted the expression of p-Nrf2 and HO-1. Moreover, PCA reversed the decreased expression of peroxisome proliferator-activated receptor γ coactivator 1α and significantly increased the mitochondrial density. Collectively, these results demonstrated that PCA attenuated PA-induced oxidative damage in HUVECs via an AMPK-dependent pathway.

摘要

原儿茶酸(PCA,3,4-二羟基苯甲酸)是花青素的主要代谢物,广泛分布于水果和蔬菜中,具有很强的抗氧化活性。在此,我们旨在研究 PCA 对高棕榈酸(PA)诱导的氧化损伤的保护作用及其在人脐静脉内皮细胞(HUVEC)中的潜在分子机制。PCA 降低了细胞内活性氧和丙二醛的水平,提高了内源性抗氧化酶的活性,包括超氧化物歧化酶、谷胱甘肽过氧化物酶 1 和血红素加氧酶 1(HO-1)。代谢组学分析表明,PCA 影响了许多代谢物,特别是一些与能量代谢有关的代谢物。PCA 还通过激活肝激酶 B1 使 AMPK 在 Thr 位点磷酸化,从而促进 p-Nrf2 和 HO-1 的表达,上调 AMPK 的活性。此外,PCA 逆转了过氧化物酶体增殖物激活受体 γ 共激活因子 1α 的表达下调,并显著增加了线粒体密度。综上所述,这些结果表明 PCA 通过 AMPK 依赖性途径减轻了 HUVEC 中 PA 诱导的氧化损伤。

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