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Tytuł pozycji:

Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells.

Tytuł:
Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells.
Autorzy:
Cao H; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Jia Q; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Yan L; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Chen C; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Xing S; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Shen D; Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 365C Xiangyang South Road, Xuhui, Shanghai 200031, China.
Źródło:
International journal of molecular sciences [Int J Mol Sci] 2019 Dec 03; Vol. 20 (23). Date of Electronic Publication: 2019 Dec 03.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:
Disease Progression*
Atherosclerosis/*pathology
Autophagy/*drug effects
Foam Cells/*metabolism
Foam Cells/*pathology
Hepatocyte Growth Factor/*metabolism
Lipoproteins, LDL/*pharmacology
Proto-Oncogene Proteins/*metabolism
Quercetin/*pharmacology
Adenine/analogs & derivatives ; Adenine/pharmacology ; Animals ; Cell Survival/drug effects ; Cellular Senescence/drug effects ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Foam Cells/drug effects ; Lipid Metabolism/drug effects ; Mice ; RAW 264.7 Cells ; Sirolimus/pharmacology ; Up-Regulation/drug effects
References:
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Grant Information:
Letter [2019] No. 128 National Traditional Chinese Medicine Innovation Talent Training Project; grant no. Y201858 and Y201934 Shanghai University of Traditional Chinese Medicine graduate "innovation ability training" special research project; grant no. 81873348 National Natural Science Foundation of China
Contributed Indexing:
Keywords: RAW264.7; atherosclerosis; autophagy; quercetin; senescence
Substance Nomenclature:
0 (Cyclin-Dependent Kinase Inhibitor p16)
0 (Cyclin-Dependent Kinase Inhibitor p21)
0 (Lipoproteins, LDL)
0 (Proto-Oncogene Proteins)
0 (macrophage stimulating protein)
0 (oxidized low density lipoprotein)
5142-23-4 (3-methyladenine)
67256-21-7 (Hepatocyte Growth Factor)
9IKM0I5T1E (Quercetin)
JAC85A2161 (Adenine)
W36ZG6FT64 (Sirolimus)
Entry Date(s):
Date Created: 20191211 Date Completed: 20200416 Latest Revision: 20200416
Update Code:
20240105
PubMed Central ID:
PMC6928812
DOI:
10.3390/ijms20236093
PMID:
31816893
Czasopismo naukowe
Objective: To investigate the process by which quercetin suppresses atherosclerosis by upregulating MST1-mediated autophagy in RAW264.7 macrophages.
Methods: An in vitro foam cell model was established by culturing RAW264.7 macrophages with oxidized low-density lipoprotein (ox-LDL). The cells were treated with quercetin alone or in combination with the autophagy inhibitor, 3-methyladenine, and autophagy agonist, rapamycin. Cell viability was detected with a CCK-8 kit. Lipid accumulation was detected by oil red O staining, senescence was detected by SA-β-gal (senescence-associated β-galactosidase) staining, reactive oxygen species were detected by ROS assay kit. Autophagosomes and mitochondria were detected by transmission electron microscope (TEM), and expression of MST1, LC3-II/I, Beclin1, Bcl-2, P21, and P16 were detected by immunofluorescence and Western blot.
Results: Ox-LDL induced RAW264.7 macrophage-derived foam cell formation, reduced survival, aggravated cell lipid accumulation, and induced a senescence phenotype. This was accompanied by decreased formation of autophagosome; increased expression of P53, P21, and P16; and decreased expression of LC3-II/I and Beclin1. After intervention with quercetin, the cell survival rate was increased, and lipid accumulation and senescence phenotype were reduced. Furthermore, the expression of LC3-II/I and Beclin1 were increased, which was consistent with the ability of quercetin to promote autophagy. Ox-LDL also increased the expression of MST1, and this increase was blocked by quercetin, which provided a potential mechanism by which quercetin may protect foam cells against age-related detrimental effects.
Conclusion: Quercetin can inhibit the formation of foam cells induced by ox-LDL and delay senescence. The mechanism may be related to the regulation of MST1-mediated autophagy of RAW264.7 cells.
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