Protective effect of Biyan Qingdu Granules on inflammatory injury of radioactive oral mucositis of nasopharyngeal carcinoma and its mechanism
Objective To observe the protective effect of Biyan Qingdu Granules(BQG)on radiotherapy-induced oral mucosal injury in rats and to explore its possible mechanism of action.Methods An F344 rat implantation tumor model was established by subcutaneous injection of FAT cells.F344 rats were divided into the control group,control radiation group,model group,and BQG low,medium,and high dose(1,2,and 4 g·kg-1)groups.Except for the control group,the animals in each group were subjected to X-ray irradiation at a radiation dose of 10 Gy·d-1 for five consecutive days.Three dose groups of BQG were subjected to pharmacological intervention after the first day of modeling,and the drug was administered by gavage once a day for 28 consecutive days.The remaining three groups were given equal volumes of distilled water.The rats in each group were subjected to general observation daily and weighed periodically.The rats were executed 24 h after the last administration.The oral mucosa and plasma of rats in each group were collected.The enzyme-linked immunosorbent assay(ELISA)detected interleukin-6(IL-6),interleukin 1β(IL-1β),and tumor necrosis factor α(TNF-α)in the plasma of rats.Western blotting detected the oral mucosa NF-κB p65,p-P65,MAPK,ERK,p-ERK,and other protein expression,and histopathological examination.Results The low,medium,and high dose groups of BQG could increase the body weight growth rate of rats;The administration groups of BQG could significantly reduce the levels of IL-6,IL-1 β,and TNF-α in the tissues of the oral light mucous membranes(P<0.05,0.01,respectively).Compared with the model group,the administration groups of BQG could significantly reduce the protein expression of MAPK,and the ratios ofp-p65/p65,p-ERK/ERK ratio were significantly reduced(P<0.05,0.01).Conclusion BQG have a therapeutic effect on radioactive oral mucositi,which may be related to reducing the level of oral mucosal inflammatory factors by regulating the NF-κB/MAPK/ERK signaling pathway.