Astragaloside IV ameliorates radiation-induced senescence via antioxidative mechanism

Author:

Liu Xin1ORCID,Shang Shuying1,Chu Weiwei1,Ma Liang1,Jiang Chenxin1,Ding Yanping2,Wang Jianlin1,Zhang Shengxiang1,Shao Baoping1

Affiliation:

1. School of Life Sciences, Lanzhou University, Lanzhou, Gansu Province, China

2. School of Life Sciences, Northwest Normal University, Lanzhou, Gansu Province, China

Abstract

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.

Publisher

Oxford University Press (OUP)

Subject

Pharmaceutical Science,Pharmacology

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