3173 - Pathological Features of Radiation-Induced Liver Disease in a Normal Rat Model

05:00pm - 06:00pm PT

Hall F

Screen: 18

POSTER

Presenter(s)

Feng Zhao, MD, PhD - The First affiliated Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang

Y. Jiang¹, J. Wu¹, F. Wang¹, W. Zhong², Z. LU¹, S. Yan¹, and F. Zhao¹; ¹Department of Radiation Oncology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China, ²Department of Pathology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

Purpose/Objective(s):

Radiation-induced liver disease (RILD) is a dose-limiting toxicity in stereotactic body radiotherapy (SBRT) for hepatocellular carcinoma (HCC). Understanding the pathological progression of RILD in normal livers is crucial for optimizing radiotherapy strategies. This study established a rat model to investigate the pathological changes associated with RILD.

Materials/Methods:

Eight male Sprague-Dawley rats were included as the normal control group. Thirty-four male Sprague-Dawley rats underwent partial liver irradiation with a dose of 25 Gy to the right liver lobe. Liver tissues were harvested at 2, 4, 8, and 12 weeks post-irradiation for histopathological analysis using HE staining, Masson’s trichrome staining, Picro-Sirius Red staining, TGF-ß immunohistochemistry, and a-SMA immunohistochemistry. Key histopathological features, including hepatocellular injury and fibrosis, were systematically evaluated.

Results:

The RILD model demonstrated time-dependent pathological progression. Early changes (2 weeks post-irradiation) included mild cellular edema and hepatocyte misalignment. By 8–12 weeks, significant collagen deposition was observed. TGF-ß and a-SMA expression indicated limited hepatic stellate cell activation, while inflammation remained minimal throughout. The findings suggest that fibrosis in this model may involve multiple mechanisms, including potential contributions from endothelial injury, though further investigation is required to confirm this.

Conclusion:

This study provides a reproducible rat model for studying RILD in a normal liver context, revealing progressive fibrosis and hepatocellular damage. These results offer a foundation for future research into the mechanisms underlying RILD and the development of mitigation strategies for SBRT in HCC patients. This study has been supported by the National Natural Science Foundation of China (82171890).