Abstract:

BACKGROUND: Polypeptide from Chlamys farreri (PCF) exerts protective effects on ultraviolet B radiation-induced human keratinocyte cell line HaCaT cells through Fas pathway and nuclear factor-κB pathway.
OBJECTIVE: To investigate HaCaT cell apoptosis after ultraviolet B radiation, and activation of tumor necrosis factor-α/ tumor necrosis factor receptor-1, and intervention of PCF.
METHODS: Cell injury models were established by 20 mJ/cm2 ultraviolet B radiation on HaCaT cells for 0.5 hour. Low-dose, moderate-dose and high-dose drug groups, positive control group and inhibitor group were treated with 1.42, 2.84, 5.69 mmol/L PCF, 5.68 mmol/L vitamin C and 50 mg/L anti- tumor necrosis factor-α monoclonal antibody.
RESULTS AND CONCLUSION: After ultraviolet B radiation, HaCaT cell apoptosis became more. Tumor necrosis factor-α, tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression increased. 1.42, 2.84 and 5.69 mmol/L PCF could reduce ultraviolet B radiation-induced tumor necrosis factor-α, tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression, and inhibit cell apoptosis, especially 5.69 mmol/L PCF, which was identical to the effects of 5.68 mmol/L vitamin C. 50 mg/L anti-tumor necrosis factor-α monoclonal antibody significantly decreased ultraviolet B radiation-induced phosphorylated c-Jun N-terminal kinase expression. These suggest that PCF inhibited ultraviolet B radiation-induced HaCaT cell apoptosis by tumor necrosis factor-α/tumor necrosis factor receptor 1 pathway.