Objective To investigate the effects of Qingreshengji ointment on NLRP3 inflammasome on skin injury repair and expression levels of MPO and Hyp in rats with radioactive dermatitis. Methods Ninety healthy SD rats were selected and provided by Changsha Tianqin Company. Eighty rats were randomly divided into normal group, model group (radiation dermatitis rat model), treatment group (model+Qingreshengji ointment) and control group (model+compound tea polyphenol ointment), with 20 rats in each group. Another inhibitor group (NLRP3 inhibitor) consisted of 10 subjects. Wound healing was measured by wound healing rate. The ultrastructure of wound tissue was observed by transmission electron microscope. Histopathological changes of wound skin were observed by HE staining. The activity of MPO was determined by spectrophotometric colorimetry. NLRP3 and Caspase-1 were detected by western blotting.Results There was no difference in wound healing among all groups on day 1 after treatment (P>0.05). The wound healing of model group was lower than that of treatment group and control group at 3-21 d (P<0.05). There was no difference in wound healing between the treatment group and the control group at each time point of 3-21 d (P>0.05). Compared with normal group, MPO expression was increased and Hyp expression was decreased in model group (P<0.05). Compared with model group, MPO expression was decreased and Hyp expression was increased in treatment group (P<0.05). There were no differences in MPO and Hyp expression between treatment group and control group (P>0.05). Compared with normal group, the expressions of NLRP3 and Caspase-1 in model group were increased (P<0.05). Compared with model group, NLRP3 and Caspase-1 protein expressions in treatment group were decreased (P<0.05). There were no differences in NLRP3 and Caspase-1 protein expressions between treatment group and inhibitor group (P>0.05). Conclusion Qingre Shengji ointment can inhibit the level of MPO and promote the expression of Hyp, and has a positive effect on the repair of skin damage in rats with radiation dermatitis. Its mechanism of action may be related to the mediation of NLRP3 inflammasome