ReferenceID 3934
Punicalagin attenuates endothelial dysfunction by activating FoxO1, a pivotal regulating switch of mitochondrial biogenesis
Free Radic Biol Med
Accumulating evidence has elucidated that hyperlipidemia is closely associated with an increasing prevalence of CVDs (cardiovascular diseases) because of endothelial dysfunction. In the present study, we investigated the
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- Reference Id
- 3934
- Evidence Id
- 20524
- Core Evidence Id
- 20524
- Source Reference Id
- 1135
- Herb2 Reference Id
- HBREF001918
- Subject Paper Key
- HBIN041294_30878647
- Pubmed Id
- 30878647
- Doi
- 10.1016/j.freeradbiomed.2019.03.011
- Paper Title
- Punicalagin attenuates endothelial dysfunction by activating FoxO1, a pivotal regulating switch of mitochondrial biogenesis
- Paper Abstract
- Accumulating evidence has elucidated that hyperlipidemia is closely associated with an increasing prevalence of CVDs (cardiovascular diseases) because of endothelial dysfunction. In the present study, we investigated the effect and mechanism of PU (Punicalagin), a major ellagitannin in pomegranate, on endothelial dysfunction both in vivo and in vitro. In vivo, PU significantly ameliorated hyperlipidemia-induced accumulation of serum triglyceride and cholesterol as well as endothelial and mitochondrial dysfunction of thoracic aorta. Intriguingly, the FoxO1 (forkhead box O1) pathway was activated, which may account for prevention of vascular dysfunction and mitochondrial loss via upregulating mitochondrial biogenesis. In line, through in vitro cell cultures, our study demonstrated that PU not only increased the total FoxO1 protein, but also enhanced its nuclear translocation. In addition, silencing of FoxO1 remarkably abolished the ability of PU to augment the mitochondrial biogenesis, eNOS (endothelial NO synthase) expression, and oxidative stress, implying the irreplaceable role of FoxO1 in regulating endothelial function in the presence of PU. Conversely, suppression of excessive ROS (reactive oxygen species) secured the PA (palmitate)-induced decrease of FoxO1 expression, implying that there was a cross-talk between FoxO1 pathway and ROS. Concomitantly, the inflammatory response in current study was primarily mediated via p38 MAPK/NF-κB signaling pathway besides of FoxO1 pathway. Taken together, our findings suggest that PU ameliorates endothelial dysfunction by activating FoxO1 pathway, a pivotal regulating switch of mitochondrial biogenesis.
- Journal
- Free Radic Biol Med
- Publish Year
- 2019
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Hyperlipidemia
- Paper Title Cn
- Paper Title En
- Punicalagin attenuates endothelial dysfunction by activating FoxO1, a pivotal regulating switch of mitochondrial biogenesis
- Bilingual Status
- semi_complete