Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway
Overexpression of miR22 induces senescence in 30PD 2BS fibroblasts which is partially rescued by salidroside (SAL). (a) Cell morphology was analyzed with fluorescence microscopy at day 3 after infection. GFP-labeled cells indicate infected cells. (b) Relative quantitation of the miR-22 expression in 30PD 2BS cells transfected with Lenti-Pre22 (MOI of 5) was analyzed by qRT-PCR analysis, relative to that in control- (Lenti-C-) transfected cells set at 1. (c) SA-β-gal activity was analyzed by phase-contrast microscopy at day 4 after infection with control vector (Lenti-C) or Pre-miR-22 (Lenti-Pre22) and effect of SAL (10 μM) on SA-β-gal staining in Lenti-Pre22-transfected 2BS cells at 30PD. (d) The percentage of SA-β-gal-positive cells. (e) The protein expression of SIRT1 and cellular senescence molecules including p53, p21, p16, and Rb in 2BS cells transfected with control vector (Lenti-C) or Pre-miR-22 (Lenti-Pre22) and effect of SAL (10 μM) Lenti-Pre22-transfected 2BS cells at 30PD. Representative images were acquired from three repeated experiments. (f) Quantitative analysis of the protein levels of SIRT1, p53, p21, Rb, and p16. versus Lenti-C; versus Lenti-C; # versus Lenti-Pre22; ## versus Lenti-Pre22.
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