放射性皮肤损伤是癌症放疗或意外接触辐射的常见并发症。本研究的目的是调查胆汁酸（BA）及其衍生物在放射性皮肤损伤期间的代谢情况。我们采用X射线直线加速器照射大鼠皮肤组织，并使用液相色谱质谱（LC-MS）定量分析对胆汁酸及其衍生物进行了测定。通过分析患者和动物模型的单细胞RNA测序（scRNA-Seq）数据，我们得出了BA生物合成关键酶在放射性皮肤损伤中的情况。我们还发现去氧胆酸（DCA）在受辐射的SD大鼠体内具有抗放射性损伤的效果。 在放射性皮肤损伤进展过程中，共有12种BA代谢产物显示出显著差异。其中，胆酸（CA）、去氧胆酸（DCA）、鼠胆酸（MCA）、炔甾醇胆酸（CDCA）、甘胆酸（GCA）、甘烯去氧胆酸（GHCA）、12-酮炔甾胆酸（12-ketoLCA）和熊去氧胆酸（UDCA）在受辐射的皮肤中显著升高，而迷胆酸（LCA）、牛磺基-β-鼠胆酸（TβMCA）和牛磺胆酸（TCA）则显著降低。此外，scRNA-Seq的结果显示，参与BA合成的7α-羟化过程的基因在皮肤成纤维细胞或角质细胞中表达出明显改变。在电离辐射后，替代的BA合成途径比经典途径更活跃地发生改变。在大鼠放射性皮肤损伤模型中，DCA促进了伤口愈合并减轻了表皮过度增生。 电离辐射调节了胆汁酸的代谢。DCA是一种有前景的治疗剂，可用于治疗放射性皮肤损伤。

Radiogenic skin injury is a common complication during cancer radiotherapy or accidental exposure to radiation. The aim of this study is to investigate the metabolism of bile acids (BA) and their derivatives during radiogenic skin injury.Rat skin tissues were irradiated by an X-ray linear accelerator. The quantification of bile acids and their derivatives were performed by liquid chromatography-mass spectrometry (LC-MS)-based quantitative analysis. Key enzymes in BA biosynthesis were analyzed from single-cell RNA sequencing (scRNA-Seq) data of radiogenic skin injury in the human patient and animal models. The in vivo radioprotective effect of deoxycholic acid (DCA) was detected in irradiated SD rats.12 BA metabolites showed significant differences during the progression of radiogenic skin injury. Among them, the levels of cholic acid (CA), deoxycholic acid (DCA), muricholic acid (MCA), chenodeoxycholic acid (CDCA), glycocholic acid (GCA), glycohyodeoxycholic acid (GHCA), 12-ketolithocholic acid (12-ketoLCA) and ursodeoxycholic acid (UDCA) were significantly elevated in irradiated skin, whereas lithocholic acid (LCA), tauro-β-muricholic acid (TβMCA) and taurocholic acid (TCA) were significantly decreased. Additionally, the results of scRNA-Seq indicated that genes involved in 7a-hydroxylation process, the first step in BA synthesis, showed pronounced alterations in skin fibroblasts or keratinocytes. The alternative pathway of BA synthesis is more actively altered than the classical pathway after ionizing radiation. In the model of rat radiogenic skin damage, DCA promoted wound healing and attenuated epidermal hyperplasia.Ionizing radiation modulates the metabolism of bile acids. DCA is a prospective therapeutic agent for the treatment of radiogenic skin injury.