When radiotherapy is administered to head and neck tumor patients, the oral mucosal epithelium is particularly damaged in radiotherapy as a fast-renewing tissue. After the oral mucosa is irradiated by radiation, when the effect of radiation on oral mucosal epithelial cells reaches a certain cumulative amount, the cell proliferation slows down, degenerates and falls off significantly, the endothelial cells of small blood vessels are damaged and occluded, the integrity of the mucosa is damaged, and microorganisms invade and lead to mucosal inflammation, together with The salivary glands are often inevitably irradiated, and the apoptosis of plasma cells causes a significant decrease in salivary secretion and a decrease in the self-cleaning effect of the oral cavity, which in turn leads to inflammatory changes in the oral mucosa and a decrease in the ability of tissue cells to regenerate and repair, resulting in mucosal congestion and edema, ulceration, white film formation, pain, and difficulty in swallowing. In addition to direct damage to the oral mucosa, radiation also causes swelling of the walls of the microvascular vessels in the radiation field, narrowing or blocking the lumen, resulting in poor blood supply to the damaged area, and even bleeding from oral mucosal ulcers in severe cases. Therefore, after about 1 week of radiation treatment, oral mucositis will appear, and when the dose reaches 30-40 GY, the reaction will spread to the entire oral mucosa. As a pleiotropic cytokine, interleukin-11 can selectively reduce the expression of inflammatory factors, promote the healing of damaged epithelial cells, and reduce the incidence of chemotherapy-induced infections, providing a new option for the treatment of oral mucositis. It was found that epithelial cells can express interleukin-11 and interleukin-11 receptor. In some damaged tissues, epithelial cells secrete large amounts of interleukin-11, which can selectively reduce the expression of pro-inflammatory factors such as TNF-α, IL-1β and interferon, regulate the activity of macrophages and T cells through immunomodulatory effects, and reduce the appearance of various pro-inflammatory mediators; interleukin-11, by inhibiting apoptosis and increasing the mitotic activity of epithelial stem progenitor cells Interleukin-11 promotes cell proliferation and inhibits apoptosis by inhibiting apoptosis and increasing mitotic activity of epithelial stem progenitor cells, significantly promoting the entry of epithelial cells from quiescence into the cell cycle after irradiation, accelerating DNA synthesis and mitotic progression.