Department of Radiation Oncology, First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, Fujian, China; Key Laboratory of Radiation Biology (Fujian Medical University), Fujian Province University, Fuzhou 350005, Fujian, China; Fujian Key Laboratory of Individualized Active Immunotherapy, Fujian Medical University, Fuzhou 350005, Fujian, China.
Central Research Lab, First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, Fujian, China; Key Laboratory of Radiation Biology (Fujian Medical University), Fujian Province University, Fuzhou 350005, Fujian, China; Fujian Key Laboratory of Individualized Active Immunotherapy, Fujian Medical University, Fuzhou 350005, Fujian, China.
Environ Toxicol Pharmacol. 2018 Jun;60:82-90. doi: 10.1016/j.etap.2018.04.012. Epub 2018 Apr 13.
Radiation-induced inflammation plays an important role in radiation-induced tissue injury. 18β-glycyrrhetinic acid (18β-GA) has shown an anti-inflammatory activity. This study aimed to assess the activity of 18β-GA against radiation-induced skin damage, and explore the underlying mechanisms. In vitro assay revealed 18β-GA treatment decreased the production of IL-1β, IL-6, PGE2 and decreased p38MAPK phosphorylation, DNA-binding activity of AP-1, and NF-κB activation in irradiated RAW264.7 macrophages. Additionally, 18β-GA suppressed NF-κB activation by inhibiting NF-κB/p65 and IκB-α phosphorylation and alleviated ROS overproduction in irradiated RAW264.7 macrophages. In vivo assay showed 18β-GA alleviated severity of radiation-induced skin damage, reduced inflammatory cell infiltration and TNF-α, IL-1β and IL-6 levels in cutaneous tissues. Our findings demonstrate that 18β-GA exhibits anti-inflammatory actions against radiation-induced skin damage probably by inhibiting NADPH oxidase activity, ROS production, activation of p38MAPK and NF-κB signaling, and the DNA binding activities of NF-κB and AP-1, consequently suppressing pro-inflammatory cytokine production.
辐射诱导的炎症在辐射诱导的组织损伤中起着重要作用。18β-甘草次酸（18β-GA）具有抗炎活性。本研究旨在评估 18β-GA 对辐射诱导皮肤损伤的作用，并探讨其潜在机制。体外实验表明，18β-GA 处理可降低照射 RAW264.7 巨噬细胞中 IL-1β、IL-6、PGE2 的产生，并降低 p38MAPK 磷酸化、AP-1 的 DNA 结合活性和 NF-κB 的激活。此外，18β-GA 通过抑制 NF-κB/p65 和 IκB-α 的磷酸化和减轻照射 RAW264.7 巨噬细胞中 ROS 的过度产生来抑制 NF-κB 的激活。体内实验表明，18β-GA 可减轻辐射诱导的皮肤损伤的严重程度，减少皮肤组织中 TNF-α、IL-1β 和 IL-6 的水平。我们的研究结果表明，18β-GA 对辐射诱导的皮肤损伤具有抗炎作用，可能是通过抑制 NADPH 氧化酶活性、ROS 产生、p38MAPK 和 NF-κB 信号通路的激活以及 NF-κB 和 AP-1 的 DNA 结合活性，从而抑制促炎细胞因子的产生。
