Frontiers in immunology · 2026
Transcriptomic profiling identifies NLRP3-associated inflammatory signatures in acute radiation enteritis and characterizes the protective effects of Qing Hua Yi Chang formula.
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Qin Yuanyuan, Li Jing, Qiu Yifan, Chang Jianming, Li Li, Wu Mianhua, Mao Cui
Аннотация
BACKGROUND: Acute radiation enteritis (ARE) is a common complication of abdominal or pelvic radiotherapy characterized by inflammatory activation and epithelial barrier dysfunction. However, the molecular mechanisms underlying ARE remain incompletely understood. This study investigated transcriptomic alterations associated with ARE and evaluated the protective effects of Qing Hua Yi Chang Formula (QHYCF).
METHODS: A murine model of ARE was established using abdominal irradiation followed by QHYCF treatment. Histopathological analysis, TUNEL staining, RT-qPCR, western blotting, and ELISA were performed to assess intestinal injury and inflammatory responses. Transcriptomic profiling combined with bioinformatic analyses was used to identify inflammatory signatures and pathways associated with ARE.
RESULTS: QHYCF attenuated radiation-induced intestinal injury, particularly at the medium dose. Transcriptomic analysis revealed dysregulation of immune- and inflammation-related pathways after irradiation and identified NLRP3-associated inflammatory signaling as a prominent inflammatory alteration in ARE. QHYCF treatment was associated with reduced NLRP3 expression and decreased serum levels of IFN-γ, IL-1β, and IL-18. In addition, QHYCF partially restored Claudin-1 expression, suggesting improvement in epithelial barrier integrity.
CONCLUSION: ARE progression is closely associated with inflammatory activation and epithelial barrier disruption. NLRP3-associated inflammatory alterations and Claudin-1 changes may represent molecular features associated with radiation-induced intestinal injury. QHYCF was associated with attenuation of inflammatory responses and preservation of epithelial barrier integrity.
METHODS: A murine model of ARE was established using abdominal irradiation followed by QHYCF treatment. Histopathological analysis, TUNEL staining, RT-qPCR, western blotting, and ELISA were performed to assess intestinal injury and inflammatory responses. Transcriptomic profiling combined with bioinformatic analyses was used to identify inflammatory signatures and pathways associated with ARE.
RESULTS: QHYCF attenuated radiation-induced intestinal injury, particularly at the medium dose. Transcriptomic analysis revealed dysregulation of immune- and inflammation-related pathways after irradiation and identified NLRP3-associated inflammatory signaling as a prominent inflammatory alteration in ARE. QHYCF treatment was associated with reduced NLRP3 expression and decreased serum levels of IFN-γ, IL-1β, and IL-18. In addition, QHYCF partially restored Claudin-1 expression, suggesting improvement in epithelial barrier integrity.
CONCLUSION: ARE progression is closely associated with inflammatory activation and epithelial barrier disruption. NLRP3-associated inflammatory alterations and Claudin-1 changes may represent molecular features associated with radiation-induced intestinal injury. QHYCF was associated with attenuation of inflammatory responses and preservation of epithelial barrier integrity.