Salidroside mitigates hydrogen peroxide-induced injury by enhancement of microRNA-27a in human trabecular meshwork cells

• Published in: Artificial cells, nanomedicine, and biotechnology Vol. 47; no. 1; pp. 1758 - 1765
• Main Authors: Zhao, Jun, Du, Xiujuan, Wang, Meng, Yang, Peiyao, Zhang, Juanmei
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.12.2019; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Apoptosis; Apoptosis - drug effects; Caspase-3; Cell viability; Cholecystokinin; Cytoprotection - drug effects; Damage assessment; Flow cytometry; Gene Expression Regulation - drug effects; Glaucoma; Glucosides - pharmacology; Humans; Hydrogen peroxide; Hydrogen Peroxide - pharmacology; Injuries; microRNA-27a; MicroRNAs - genetics; miRNA; Oxidative Stress - drug effects; Phenols - pharmacology; Phosphatidylinositol 3-Kinases - metabolism; PI3K/AKT; Proto-Oncogene Proteins c-akt - metabolism; Ribonucleic acid; RNA; Salidroside; Trabecular Meshwork - cytology; Trabecular Meshwork - drug effects; Trabecular Meshwork - metabolism; Wnt protein; Wnt Signaling Pathway - drug effects; Wnt/β-catenin; β-Catenin; Glaucoma; Salidroside; microRNA-27a; Wnt/β-catenin; hydrogen peroxide; PI3K/AKT
• ISSN: 2169-1401; 2169-141X
• DOI: 10.1080/21691401.2019.1608222

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.