ArticleFood science of animal resources2020
Duck Oil-loaded Nanoemulsion Inhibits Senescence of Angiotensin II-treated Vascular Smooth Muscle Cells by Upregulating SIRT1.
Article in Food science of animal resources, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Paeonol Attenuates Atherosclerosis by Inhibiting Vascular Smooth Muscle Cells Senescence via SIRT1/P53/TRF2 Signaling Pathway.Molecules (Basel, Switzerland) · 2024Article
- Effect of sous-vide cooking conditions on the physicochemical, microbiological and microstructural properties of duck breast meat.Animal bioscience · 2023Article
- SIRT1 pathway in Parkinson's disease: a faraway snapshot but so close.Inflammopharmacology · 2023Review
- Effects of Chitosan and Duck Fat-Based Emulsion Coatings on the Quality Characteristics of Chicken Meat during Storage.Foods (Basel, Switzerland) · 2022Article
- HSP27 role in cardioprotection by modulating chemotherapeutic doxorubicin-induced cell death.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Physiochemical properties of reduced-fat duck meat emulsion systems: effects of preemulsification with vegetable oils and duck skin.Poultry science · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is associated with age-related vascular disorders and has been implicated in vascular dysfunctions. Here, we show that duck oil-loaded nanoemulsion (DO-NE) attenuates premature senescence of vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II). Compared with control nanoemulsion (NE), DO-NE significantly inhibited the activity of senescence-associated β-galactosidase, which is a biomarker of cellular senescence, in Ang II-treated VSMCs. SIRT1 protein expression was dose- and time-dependently induced in VSMCs exposed to DO-NE, but not in those exposed to NE, and SIRT1 promoter activity was also elevated. Consistently, DO-NE also dose-dependently rescued Ang II-induced repression of SIRT1 expression, indicating that SIRT1 is linked to the anti-senescence action of DO-NE in VSMCs treated with Ang II. Furthermore, the SIRT1 agonist resveratrol potentiated the effects of DO-NE on VSMCs exposed to Ang II, whereas the SIRT1 inhibitor sirtinol elicited the opposite effect. These findings indicate that DO-NE inhibits senescence by upregulating SIRT1 and thereby impedes vascular aging triggered by Ang II.
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