Inflammatory response of thymus bystander effects on acute radiation-induced skin injury in rats

Radiation not only kills tumor cells, but also damages other sites. The mechanisms of damage caused by the bystander effect of irradiation in animal models are unclear and the time node is single. In this study, we aimed to investigate the inflammatory response of thymus tissue injury in non-irradiated areas at different times after irradiating rat skin.

Rats were irradiated with an X-ray dose of 38 Gy, and at 15 d after irradiation, when the skin wound was most severe, the pro-inflammatory drug high mobility group box1 (HMGB1) and the anti-inflammatory drug glycyrrhizic acid (GA) were injected intraperitoneally into rats. After irradiation, skin tissues were collected for histology, and thymus tissues were collected for gene and protein testing.

Animal model of skin damage was successfully established. The expression of macrophage (F4/80) increased after irradiation, and F4/80 produced cytokines. Through the flow which was activated by inflammatory factors in the blood, DNA damage and the expression of inflammatory-related cytokines in non-irradiated area of the thymus peaked at 15 d after irradiation. Moreover, HMGB1 treatment increased the expression at 1 d after intraperitoneal injection, and GA solution decreased the expression of inflammatory-related cytokines.

When radiation damages the skin, it can cause damage to other organs through the circulation, and an anti-inflammatory GA solution reduced inflammatory responses, which are required to modify radiation-induced systemic effects with anti-inflammatory drugs or agents that affect pathways that cause bystander instability.