Radiation-induced skin injury is a common side effect of radiotherapy, but there are few therapeutic drugs available for prevention or treatment. In this study, we demonstrate that 18β-Glycyrrhetinic acid (18β-GA), a bioactive component derived from Glycyrrhiza glabra , substantially reduces the accumulation of reactive oxygen species (ROS) and inhibits apoptosis in HaCaT cells after ionizing radiation (IR), thereby mitigating radiation-induced skin injury. Mechanistically, 18β-GA promotes the nuclear import of Nrf2, leading to activation of the Nrf2/HO-1 signaling pathway in response to IR. Importantly, Nrf2 silencing increases cell apoptosis and reverse the protective effect of 18β-GA on radiation-induced skin injury. Furthermore, 18β-GA preserves skin tissue structure after irradiation, inhibits inflammatory cell infiltration, and alleviates radiation dermatitis. In conclusion, our results suggest that 18β-GA reduces intracellular ROS production and apoptosis by activating the Nrf2/HO-1 signaling pathway, leading to amelioration of radiation dermatitis.
Keyphrases
- radiation induced
- signaling pathway
- oxidative stress
- pet ct
- pi k akt
- cell cycle arrest
- induced apoptosis
- reactive oxygen species
- radiation therapy
- soft tissue
- cell death
- wound healing
- dna damage
- endoplasmic reticulum stress
- epithelial mesenchymal transition
- cell proliferation
- mouse model
- single cell
- early stage
- squamous cell carcinoma
- cell therapy
- bone marrow
- mesenchymal stem cells
- combination therapy