Model of HaCaT cell injury induced by 60Co γ-rays and the underlying mechanism

Abstract

The aim of this study was to investigate the damage caused to HaCaT cells by 60Co γ-rays at different doses and the underlying mechanism and to establish a cell model of radiation-induced skin injury. HaCaT cells were irradiated with a single dose of 60Co γ-rays (the radiation source was 3 m away from the cells, and the dose rate was 100.68 cGy/min). The cell activity was detected using the CCK-8 method, the vitality of superoxide dismutase (SOD) was measured using the water soluble tetrazolium salt staining method, the malondialdehyde (MDA) level was determined using the thiobarbituric acid method, the apoptosis rate was monitored through flow cytometry, and the expression of the apoptosis- and inflammation-related proteins was detected via western blotting. After irradiation with 60Co γ-rays at 18 Gy for 24 h, the morphology of HaCaT cells changed significantly, cell activity decreased to 57.5%, MDA level increased to 66.28 µmol/mg, inhibition rate of SOD increased to 32.12%, apoptosis rate increased to 18.05%, and expression of inflammatory factors increased. After incubation for 24 h at an absorbed dose of 18 Gy, the cellular models of radiation-induced skin injury were established. The mechanism of cell injury may be related to cell oxidative damage, apoptosis, and inflammatory reaction.

Keywords

• radiation-induced skin injury
• 60co γ-ray
• oxidative damage
• apoptosis
• inflammatory reaction