Fucoxanthin Protects against oxLDL-Induced Endothelial Damage via Activating the AMPK-Akt-CREB-PGC1α Pathway

Hsiu Chung Ou, Wan Ching Chou, Pei Ming Chu, Pei Ling Hsieh, Ching Hsia Hung, Kun Ling Tsai

研究成果: Article同行評審

12 引文 斯高帕斯(Scopus)

摘要

Scope: Atherosclerotic cardiovascular disease is the most prevalent cause of mortality and morbidity. Fucoxanthin (FX) possesses anti-hypertensive and anti-obesity properties. However, the molecular mechanisms underlying the inhibitory effects of FX on oxidized low-density lipoprotein (oxLDL)-induced oxidative injuries in human endothelial cells are still largely unknown. This study aims to test the hypothesis that FX protects against oxLDL-induced oxidative stress by upregulating AMP-activated protein kinase (AMPK) and to explore the roles of cAMP response element binding protein (CREB) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α). Methods and Results: Human umbilical vein endothelial cells are treated with oxLDL in the presence or absence of FX. FX significantly increases AMPK phosphorylation. In addition, FX diminishes oxLDL-mediated nicotinamide adenine dinucleotide phosphate oxidase activation by inhibiting protein kinase C and subsequently inducing reactive oxygen species generation and impairing the activity of the endogenous antioxidant enzyme superoxidase dismutase. Furthermore, FX restores oxLDL-mediated dephosphorylation of phosphoinositide-3-kinase/Akt and decreases CREB and PGC-1α expression to nearly normal levels. Moreover, FX ameliorates the oxLDL-mediated suppression of mitochondrial function and apoptosis. Conclusion: These findings provide new insights into the possible molecular mechanisms by which FX mitigates oxLDL-induced endothelial oxidative stress and mitochondrial dysfunction.

原文English
文章編號1801353
期刊Molecular Nutrition and Food Research
63
發行號10
DOIs
出版狀態Published - 2019 五月

All Science Journal Classification (ASJC) codes

  • 生物技術
  • 食品科學

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