Abstract
The aim of the present study was to investigate the role of microRNAs (miRNAs/miRs) in the anti‑fibrotic effect of astaxanthin (AST), using the human hepatic stellate cell (HSC) line LX‑2 as the research model. LX‑2 cells were treated with various concentrations of AST (10, 20 and 40 µM) for 24 or 48 h. miR‑29b was selected based on existing literature, and its targeting gene B cell lymphoma (Bcl)‑2 was predicted by TargetScan and miRanda databases for further analysis. Interactions between miR‑29b and Bcl‑2 in the AST treated LX‑2 cells were evaluated using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. MTT analysis was used to analyze cell viability. Overexpression of miR‑29b decreased the expression of Bcl‑2 in AST‑treated LX‑2 cells, and silencing of it had the opposite effect. Additionally, Annexin V‑fluorescein isothiocyanate/propidium iodide double staining and flow cytometry were used to evaluate the cell apoptosis, and overexpression of miR‑29b increased cell apoptosis rates in AST‑treated LX‑2 cells; however, silencing of it had the opposite effect. RT‑qPCR and western blotting demonstrated that AST induced LX‑2 cells apoptosis which may be by regulating miR‑29b, as indicated by inhibited Bcl‑2 expression levels and elevated Bax and Caspase‑3 expression levels. These results highlight an important role of miR‑29b in the AST modulating LX‑2 cells proliferation and apoptosis and implicate a potential mechanism of miR‑29b and AST preventing liver fibrosis.