RESUMO
Icariin (ICA) has been used as a promising antiaging drug; however, its underlying molecular mechanism is yet to be elucidated. The present study aimed to determine the antiaging molecular mechanisms of ICA. Dgalactose (Dgal) was used to generate a cell aging model. IMR90 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 Dgal (200 mmol/l) at 37ËC for 72 h. Senescence of IMR90 cells was assessed by senescenceassociatedßgalactosidase (SAßGal) 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 Dgal notably increased the proportion of SAßGalpositive cells and decreased the viability of IMR90 cells; however, pretreatment with ICA reversed the effects of Dgal on IMR90 cells in a concentrationdependent manner. Furthermore, it was also demonstrated that the activation of p53/p21 and nuclear factorκB (NFκB) signaling, and downregulation of SIRT1/6 may be involved in IMR90 cells, in Dgalinduced aging and ICA may effectively prevent IMR90 cells from these changes induced by Dgal. Taken together, the results of the present study suggest that the antiaging molecular mechanisms of ICA may be associated with the regulation of the SIRT1/NFκB pathway.