Dihydroartemisinin (DHA) is a derivative of artemisinin, which affects inflammation, oxidative stress, and immune regulation. However, the mechanism underlying its effects remains largely unknown. This study aims to explore the mechanism by which DHA affects radiation‐induced lung injury (RILI), providing new insights for lung radiotherapy. To elucidate its mechanism of action, C57BL/6 J mice were irradiated with 15 Gy whole chest. RILI was evaluated by qRT‐PCR, ELISA, histology, Western blot analysis, immunohistochemistry, and RILI signaling cascade studies. In addition, small interfering RNAs were employed to knockdown cGAS proteins in the cGAS‐STING signaling pathway in the human bronchial epithelium cell line (BEAS‐2B). Both In Vivo and Vitro experiments were conducted to investigate the specific mechanism by which DHA alleviated RILI. We observed the activation of the cGAS‐STING pathway, along with the phosphorylation of the downstream target NF‐κB and an increase in inflammatory factor levels in the mouse model following radiation exposure. In the cell model, irradiation also triggered the activation of the cGAS‐STING signaling pathway and its downstream targets, leading to elevated levels of inflammatory factors. Notably, knocking down the cGAS using small interfering RNA in the BEAS‐2B cells significantly alleviated RILI in the cell model. Our study elucidated the mechanism of DHA reducing RILI through the cGAS/STING/NF‐κB signaling pathway, and revealed that the GAS/STING/NF‐κB axis may be a potential therapeutic target for RILI.

The integration of immunotherapy with neoadjuvant therapy for proficient mismatch repair (pMMR) locally advanced rectal cancer (LARC) is a promising strate

This study aimed to construct a nomogram to predict radiation-induced hepatic toxicity in patients with hepatocellular carcinoma treated with intensity-modulated radiotherapy. This study reviewed the clinical characteristics and dose–volume parameters of 196 patients with hepatocellular carcinoma. Radiation-induced hepatic toxicity was defined as progression of the Child–Pugh score caused by intensity-modulated radiotherapy. Factors relevant to radiation-induced hepatic toxicity were selected using receiver operating characteristic and univariate logistic analysis. A risk assessment model was developed, and its discrimination was validated. Eighty-eight (44.90%) and 28 (14.29%) patients had radiation-induced hepatic toxicity ≥ 1 (Child–Pugh ≥ 1) and radiation-induced hepatic toxicity ≥ 2 (Child–Pugh ≥ 2). Pre-treatment Child–Pugh, body mass index and dose–volume parameters were correlated with radiation-induced hepatic toxicity ≥ 1 using univariate logistic analysis. V15 had the best predictive effectiveness among the dose–volume parameters in both the training (area under the curve: 0.763, 95% confidence interval: 0.683–0.842, P < 0.001) and validation cohorts (area under the curve: 0.759, 95% confidence interval: 0.635–0.883, P < 0.001). The area under the curve values of the model that was constructed by pre-treatment Child–Pugh, body mass index and V15 for radiation-induced hepatic toxicity ≥1 were 0.799 (95% confidence interval: 0.719–0.878, P < 0.001) and 0.775 (95% confidence interval: 0.657–0.894, P < 0.001) in the training and validation cohorts, respectively. Patients with a body mass index ≤ 20.425, Barcelona clinic liver cancer = C, Hepatitis B Virus-positive, Eastern Cooperative Oncology Group = 1–2 and hepatic fibrosis require lower V15 dose limits. Risk assessment model constructed from Pre-treatment Child–Pugh, V15 and body mass index can guide individualized patient selection of toxicity minimization strategies.