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Intestinal Epithelial Regeneration in Response to Ionizing Irradiation
Published on: July 27, 2022
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Licochalcone D Alleviates Radiation-Induced Intestinal Injury via SIRT3-Dependent Mitophagy: A Natural Phytochemical
Jiaxin Zhang1, Shengjie Ma1, Zhen Wang1
1Department of Gastrocolorectal Surgery, General Surgery Center, The First Hospital of Jilin University, Changchun 130021, China.
Journal of Agricultural and Food Chemistry
|October 1, 2025
Summary
Licochalcone D (LCD) protects against radiation-induced intestinal injury by reducing oxidative stress. It activates the SIRT3-mitophagy pathway, preserving intestinal cells and offering a new therapeutic target.
Area of Science:
- Biomedical Sciences
- Cell Biology
- Radiation Oncology
Background:
- Ionizing radiation causes oxidative stress, leading to radiation-induced intestinal injury (RIII).
- Licochalcone D (LCD), a licorice-derived compound, has antioxidant properties, but its protective effects against RIII are not well understood.
Purpose of the Study:
- To investigate the protective role and underlying mechanism of Licochalcone D (LCD) against radiation-induced intestinal injury (RIII).
Main Methods:
- In vitro studies using intestinal epithelial cells to assess viability, DNA damage, and reactive oxygen species (ROS) levels after LCD pretreatment and radiation exposure.
- In vivo studies in mice to evaluate LCD's effects on body weight, intestinal morphology, and crypt/villous damage following irradiation.
Main Results:
- LCD pretreatment significantly improved cell viability, reduced DNA breaks, and suppressed ROS accumulation in irradiated intestinal cells.
- In vivo, LCD administration mitigated radiation-induced weight loss, preserved intestinal crypts, and reduced villous damage.
- Mechanistically, LCD was found to stabilize SIRT3, activating mitophagy to clear ROS, thereby reducing DNA damage and apoptosis.
Conclusions:
- Licochalcone D (LCD) demonstrates significant protective effects against radiation-induced intestinal injury (RIII) through an antioxidant mechanism involving the SIRT3-mitophagy pathway.
- The findings highlight LCD as a potential therapeutic agent for RIII and identify the SIRT3-mitophagy axis as a novel pharmacological target.
