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Tytuł:
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Sargahydroquinoic acid (SHQA) suppresses cellular senescence through Akt/mTOR signaling pathway.
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Autorzy:
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Cao L; Institute of Marine Life Science, Pukyong National University, Daeyeon 3-dong, Nam-gu, Busan 608-737, South Korea. Electronic address: .
Lee SG; Department of Food Science and Nutrition, Pukyong National University, Daeyeon 3-dong, Nam-gu, Busan 608-737, South Korea. Electronic address: .
Park SH; Department of Biomedical Engineering, Pukyong National University, Daeyeon 3-dong, Nam-gu, Busan 608-737, South Korea. Electronic address: .
Kim HR; Department of Food Science and Nutrition, Pukyong National University, Daeyeon 3-dong, Nam-gu, Busan 608-737, South Korea. Electronic address: .
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Źródło:
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Experimental gerontology [Exp Gerontol] 2021 Aug; Vol. 151, pp. 111406. Date of Electronic Publication: 2021 May 20.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: Tarrytown Ny : Elsevier Science
Original Publication: Oxford.
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MeSH Terms:
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Endothelial Cells*/metabolism
Proto-Oncogene Proteins c-akt*/metabolism
Alkenes ; Benzoquinones ; Cells, Cultured ; Cellular Senescence ; Humans ; Hydrogen Peroxide ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Protein p53
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Contributed Indexing:
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Keywords: Akt; Endothelial cells; Sargahydroquinoic acid; Senescence; mTOR
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Substance Nomenclature:
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0 (Alkenes)
0 (Benzoquinones)
0 (Tumor Suppressor Protein p53)
0 (sargahydroquinoic acid)
BBX060AN9V (Hydrogen Peroxide)
EC 2.7.1.1 (MTOR protein, human)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
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Entry Date(s):
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Date Created: 20210522 Date Completed: 20210702 Latest Revision: 20211204
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Update Code:
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20240105
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DOI:
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10.1016/j.exger.2021.111406
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PMID:
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34022274
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Aim: The effects of sargahydroquinoic acid (SHQA) on cellular senescence and the underlying mechanisms were investigated using human umbilical vascular endothelial cells (HUVECs).
Methods: SHQA or DMSO was supplemented into the medium. Low dose of H 2 O 2 was used to induce premature senescence. Replicative senescence was achieved by continuously culturing cells until they reached a plateau phase. Senescence biomarkers, including p53, p21, and p16 proteins, and SA-β-Gal activity were measured.
Results: Pretreatment of SHQA significantly suppressed the oxidative stress-induced protein expression of p53, p21, and p16, as well as the activity of SA-β-Gal. Additionally, SHQA also delayed the replicative senescence as indicated by an increased population doubling number, reduced protein expression of p53, p21, and p16, as well as a decreased SA-β-Gal activity. SHQA inhibited the phosphorylation of Akt, mTOR, and downstream targets of mTOR, such as p-S6K, which was elevated by premature senescence and replicative senescence. In the absence of senescence stimuli, SHQA also inhibited the Akt/mTOR signaling pathway and promoted autophagy.
Conclusions: SHQA suppressed senescence induced by oxidative stress and replication through inhibiting the Akt/mTOR pathway. With the potential of acting as an Akt/mTOR inhibitor, SHQA might be useful for developing anti-ageing therapy.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
