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Tytuł:
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Salidroside mitigates hydrogen peroxide-induced injury by enhancement of microRNA-27a in human trabecular meshwork cells.
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Autorzy:
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Zhao J; a Department of Ophthalmology , Linyi People's Hospital , Linyi , China.
Du X; b Department of Ophthalmology, Eye Institute of Shandong University of Traditional Chinese Medicine , Affiliated Eye Hospital of Shandong University of TCM , Jinan , China.
Wang M; a Department of Ophthalmology , Linyi People's Hospital , Linyi , China.
Yang P; c Qingdao University , Qingdao , China.
Zhang J; a Department of Ophthalmology , Linyi People's Hospital , Linyi , China.
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Źródło:
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Artificial cells, nanomedicine, and biotechnology [Artif Cells Nanomed Biotechnol] 2019 Dec; Vol. 47 (1), pp. 1758-1765.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: 2015- : Abingdon, Oxford : Taylor & Francis
Original Publication: London : Informa Healthcare, [2013]-
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MeSH Terms:
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Glucosides/*pharmacology
Hydrogen Peroxide/*pharmacology
MicroRNAs/*genetics
Phenols/*pharmacology
Trabecular Meshwork/*cytology
Trabecular Meshwork/*drug effects
Apoptosis/drug effects ; Cytoprotection/drug effects ; Gene Expression Regulation/drug effects ; Humans ; Oxidative Stress/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Trabecular Meshwork/metabolism ; Wnt Signaling Pathway/drug effects
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Contributed Indexing:
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Keywords: Glaucoma; PI3K/AKT; Salidroside; Wnt/β-catenin; hydrogen peroxide; microRNA-27a
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Substance Nomenclature:
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0 (Glucosides)
0 (MIRN27 microRNA, human)
0 (MicroRNAs)
0 (Phenols)
BBX060AN9V (Hydrogen Peroxide)
EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
M983H6N1S9 (rhodioloside)
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Entry Date(s):
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Date Created: 20190508 Date Completed: 20190829 Latest Revision: 20210811
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Update Code:
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20240105
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DOI:
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10.1080/21691401.2019.1608222
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PMID:
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31062616
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Salidroside (Sal) exerted widely pharmacological effects in multitudinous diseases had been certified. The actual study clarified the protective activity of Sal in H 2 O 2 -injured human trabecular meshwork (HTM) cells. HTM cells were disposed with H 2 O 2 to construct an oxidative damage model in vitro. Then, Sal was utilized to administrate HTM cells, and cell viability, apoptosis, apoptosis-interrelated proteins and ROS production were appraised using CCK-8, flow cytometry, western blot and DCFH-DA staining. MiR-27a inhibitor and its control were transfected into HTM cells, and the influences of miR-27a inhibition in HTM cells stimulated with H 2 O 2 and Sal were detected. PI3K/AKT and Wnt/β-catenin pathways were ultimately investigated to uncover the underlying mechanism. We found that H 2 O 2 evoked HTM cells oxidative damage, as evidenced by repressing cell viability, inducing apoptosis, activating cleaved-caspase-3/-9 expression and increasing ROS production. Sal significantly lightened H 2 O 2 -evoked oxidative damage in HTM cells. Additionally, miR-27a was up-regulated by Sal, and miR-27a suppression significantly reversed the protective effect of Sal on H 2 O 2 -injured HTM cells. Finally, Sal activated PI3K/AKT and Wnt/β-catenin pathways through enhancement of miR-27a in H 2 O 2 -injured HTM cells. In conclusion, these discoveries suggested that Sal could protect HTM cells against H 2 O 2 -evoked oxidative damage by activating PI3K/AKT and Wnt/β-catenin pathways through enhancement of miR-27a. Highlights H 2 O 2 evokes HTM cells oxidative damage; Sal relieves H 2 O 2 -induced oxidative damage in HTM cells; Sal enhances miR-27a expression in H 2 O 2 -injured HTM cells; Repressed miR-27a reverses the protective impacts of Sal on H 2 O 2 -injured HTM cells; Sal activates PI3K/AKT and Wnt/β-catenin pathways by increasing miR-27a.
Expression of concern in: Artif Cells Nanomed Biotechnol. 2021 Dec;49(1):553. (PMID: 34374628)
