# Studies on the Protective Effect of Silybin Against Low-Dose Radiation-Induced Damage to the Immune System

## TL;DR

This study shows that silybin can protect the immune system from damage caused by low-dose radiation, both in cells and in animals.

## Contribution

The novel contribution is demonstrating silybin's protective effects against low-dose radiation-induced immune damage and its potential mechanism via the cGAS pathway.

## Key findings

- Silybin reduced radiation-induced cell proliferation decline and ROS levels in RAW264.7 cells.
- Silybin mitigated radiation effects on body weight, blood cell counts, and spleen immune cell numbers in animals.
- Silybin decreased cGAS protein-positive cells in the spleen, suggesting a role in its protective mechanism.

## Abstract

With growing public concern about the health effects of low-dose radiation, numerous studies have demonstrated that low-dose radiation can cause damage to the immune system, making intervention measures essential. This study investigated the protective effects of silybin against low-dose radiation-induced immune system damage and its underlying mechanisms at both the cellular and animal levels. At the cellular level, CCK-8 assays, ROS measurements, and RT-qPCR analysis revealed that silybin alleviated the reduction in RAW264.7 cell proliferation, intracellular ROS levels, and inflammatory cytokine expression following low-dose radiation exposure. At the animal level, comparative analyses of post-irradiation body weight, peripheral blood cell counts, immune organ coefficients, spleen HE/IHC staining, and spleen immune cell numbers demonstrated that silybin mitigated the radiation-induced decrease in body weight, reduction in peripheral blood leukocyte counts, inflammatory cell infiltration in the spleen, decline in spleen immune cell numbers, and increase in cGAS protein-positive cells. These findings indicate that silybin exerts protective effects against low-dose radiation-induced immune system damage, potentially by regulating the cGAS signaling pathway to reduce radiation-induced cellular injury, thereby enhancing its radioprotective properties.