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Purpose <p>To optimize an animal model of acute radiation-induced esophagitis (RIE) in C57BL/6 mice and characterize the histopathological features of RIE at different stages.</p> Materials and methods <p>C57BL/6 mice were subjected to single thoracic X-ray irradiation at doses ranging from 5 to 30&#xa0;Gy. Changes in body weight, daily food and water intake, and survival were monitored and compared within 2&#xa0;weeks after radiation exposure. Epithelial damage to the esophagus, apoptosis, and inflammation at different times after irradiation were examined to characterize the pathological process of RIE.</p> Results <p>The incidence of acute RIE was strongly correlated with increasing radiation dose across all the experimental groups. No deaths were observed in mice that received 5 or 10&#xa0;Gy of irradiation, whereas complete mortality was observed within 15&#xa0;days after exposure to 30&#xa0;Gy of irradiation. The mice in 20&#xa0;Gy irradiation group had a low mortality rate. The peak of esophageal tissue damage occurred at Day 7 and was healed by Day 14 after exposure to 20&#xa0;Gy of thoracic irradiation. The pathology of RIE was induced by radiation-induced DNA damage, apoptosis, reactive oxygen species (ROS), and mitochondrial impairment.</p> Conclusions <p>In this study, we found that a single 20&#xa0;Gy thoracic irradiation was the optimal dose to establish acute RIE in C57BL/6 mice. Acute esophageal injury peaked on Day 7 after radiation, and the process of regeneration and repair was complete within 14&#xa0;days. This work may be a useful reference for experimental research concerning RIE.</p>

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Optimization and characterization of acute radiation-induced esophagitis in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Jianhua Feng,
  • Xiangjun Liu,
  • Lu Xu,
  • Ke Wang,
  • Simin He,
  • Xi Wang,
  • Yujun Huang,
  • Shubin Wang,
  • Xudan Lei,
  • Lingxiao Huang,
  • Zhenni Xu,
  • Jinyi Lang,
  • Dengqun Liu,
  • Jun Yin

摘要

Purpose

To optimize an animal model of acute radiation-induced esophagitis (RIE) in C57BL/6 mice and characterize the histopathological features of RIE at different stages.

Materials and methods

C57BL/6 mice were subjected to single thoracic X-ray irradiation at doses ranging from 5 to 30 Gy. Changes in body weight, daily food and water intake, and survival were monitored and compared within 2 weeks after radiation exposure. Epithelial damage to the esophagus, apoptosis, and inflammation at different times after irradiation were examined to characterize the pathological process of RIE.

Results

The incidence of acute RIE was strongly correlated with increasing radiation dose across all the experimental groups. No deaths were observed in mice that received 5 or 10 Gy of irradiation, whereas complete mortality was observed within 15 days after exposure to 30 Gy of irradiation. The mice in 20 Gy irradiation group had a low mortality rate. The peak of esophageal tissue damage occurred at Day 7 and was healed by Day 14 after exposure to 20 Gy of thoracic irradiation. The pathology of RIE was induced by radiation-induced DNA damage, apoptosis, reactive oxygen species (ROS), and mitochondrial impairment.

Conclusions

In this study, we found that a single 20 Gy thoracic irradiation was the optimal dose to establish acute RIE in C57BL/6 mice. Acute esophageal injury peaked on Day 7 after radiation, and the process of regeneration and repair was complete within 14 days. This work may be a useful reference for experimental research concerning RIE.