Icariin modulates the sirtuin/NF-κB pathway and exerts anti-aging effects in human lung fibroblasts

Icariin (ICA) has been used as a promising anti-aging drug; however, its underlying molecular mechanism is yet to be elucidated. The present study aimed to determine the anti-aging molecular mechanisms of ICA. D-galactose (D-gal) was used to generate a cell aging model. IMR-90 human lung fibroblasts were pretreated with different concentrations of ICA (1, 2, 4, 8 and 16 µmol/l) for 6 h and subsequently incubated with D-gal (200 mmol/l) at 37°C for 72 h. Senescence of IMR-90 cells was assessed by senescence-associated-β-galactosidase (SA-β-Gal) staining assay. Cell viability, and the expression levels of p53/p21, sirtuin (SIRT) 1/6 and p50/p65 were determined via the MTT assay and western blotting respectively. The results demonstrated that D-gal notably increased the proportion of SA-β-Gal-positive cells and decreased the viability of IMR-90 cells; however, pretreatment with ICA reversed the effects of D-gal on IMR-90 cells in a concentration-dependent manner. Furthermore, it was also demonstrated that the activation of p53/p21 and nuclear factor-κB (NF-κB) signaling, and downregulation of SIRT1/6 may be involved in IMR-90 cells, in D-gal-induced aging and ICA may effectively prevent IMR-90 cells from these changes induced by D-gal. Taken together, the results of the present study suggest that the anti-aging molecular mechanisms of ICA may be associated with the regulation of the SIRT1/NF-κB pathway.