Objective: To explore the role of Erianin in specific dermatitis (AD) and its regulatory mechanism in HMGB 1 / RAGE-RHOA / ROCK 1-signaling pathway. Methods: DNCB induced BALB/c mice serve as a model for AD. Measure the skin thickness, spleen, and lymph node weight of mice. Methylamine blue and H&E staining were used to detect pathological changes in the back skin and ears of mice. ELISA detects levels of inflammatory factors. Establishment of an in vitro model of Alzheimer"s disease using HaCaT cells stimulated by TNF - α. Use flow cytometry to detect cellular ROS. Immunofluorescence assay was used to detect mtROS. TUNEL method was used to detect cell apoptosis. Use immunoblotting to detect the expression of HMGB1, RAGE, RhoA, and ROCK1 proteins.Results: It inhibited the increase of skin thickness, reduced the weight of spleen and lymph nodes, improved the infiltration of inflammatory cells, and the degranulation of mast cells, and reduced the level of inflammatory factors. In vitro, Erianin reduced the production of cellular ROS, mtROS induced by TNF- α. The protein expression of HMGB 1, RAGE, RhoA and ROCK 1 decreased. Treatment of r-HMGB1-stimulated HaCaT cells with RAGE-specific blocker (TFA) showed no change in HMGB1 expression, and the expression of RAGE, RhoA, and ROCK1 decreased. In the Rho kinase inhibitor (Y-27632) + TNF- α group, except for RAGE, the results were similar to the TFA + TNF- α group. Conclusion: Erianin relieves atopic dermatitis by regulating the HMGB 1 / RAGE-RhoA / ROCK 1 signaling pathway.