Astragaloside IV ameliorates radiation-induced senescence via antioxidative mechanism

Abstract

Objectives Ageing is a universal and gradual process of organ deterioration. Radiation induces oxidative stress in cells, which leads to genetic damage and affects cell growth, differentiation and senescence. Astragaloside (AS)‐IV has antioxidative, anti‐apoptotic and anti‐inflammatory properties. Methods To study the protective mechanism of AS‐IV on radiation‐induced brain cell senescence, we constructed a radiation‐induced brain cell ageing model, using biochemical indicators, senescence‐associated galactosidase (SA‐β‐gal) senescence staining, flow cytometry and Western blotting to analyse the AS‐IV resistance mechanism to radiation‐induced brain cell senescence. Key findings Radiation reduced superoxide dismutase (SOD) activity and expressions of cyclin‐dependent kinase (CDK2), CDK4, cyclin E and transcription factor E2F1 proteins, and increased expressions of p21, p16, cyclin D and retinoblastoma (RB) proteins, malondialdehyde (MDA) activity, SA‐β‐gal–positive cells and cells stagnating in G1 phase. After treatment with AS‐IV, the level of oxidative stress in cells significantly decreased and expression of proteins related to the cell cycle and ageing significantly changed. In addition, SA‐β‐gal–positive cells and cells arrested in G1 phase were significantly reduced. Conclusions These data suggest that AS‐IV can antagonize radiation‐induced brain cells senescence; and its mechanism may be related to p53‐p21 and p16‐RB signalling pathways of ageing regulation.