Objective To evaluate the therapeutic effects of the Chinese herbal prescription Guomin Decoction (GMJ) on Th2-type atopic dermatitis (AD), with a focus on its potential to inhibit macrophage-mediated inflammation via the JAK1/JAK2-STAT1/STAT3 signaling pathway. Methods A total of 48 BALB/c mice were randomly assigned to six groups: the Normal group (control), the Model group (AD model), the Dexamethasone-positive control group (Dex. group), and the Guomin Decoction high-dose(GMJ-H), medium-dose(GMJ-M), and low-dose(GMJ-L) groups. Each group received its respective treatment, and outcomes were analyzed to assess the efficacy of GMJ in mitigating AD symptoms and inflammation. A mouse model of AD was established by repeatedly applying 2 nmol MC903 (Calcipotriene) to the right ear of mice. The number of scratches was recorded to observe changes in scratching behavior. Ear swelling was measured to assess inflammation, and the organ coefficient was calculated. Histological changes in skin morphology were examined using HE staining, while toluidine blue staining was employed to evaluate the number of mast cells. The serum levels of IL-4, IL-5, IL-33, TSLP, HIS, LTB4, and IgE were quantified using the ELISA method. Additionally, the tissue levels of IL-4, IL-33, and TNF-α in the skin lesions were determined through immunohistochemistry. RAW264.7 cells were cultured in vitro to evaluate the effects of Guomin Decoction on cell viability using the MTT assay. Experimental groups included Control, Model, GMJ-94(94 μg/mL), GMJ-187(187 μg/mL), and GMJ-375(375 μg/mL). A macrophage inflammation model was established by stimulating RAW264.7 cells with 1 μg/mL LPS. After 24 hours of stimulation, the cell culture supernatant was collected for analysis. Nitric oxide(NO) levels were measured using the Griess method, while IL-6 concentrations were determined by ELISA. Western blot analysis was performed to detect the expression of phosphorylated JAK1, JAK2, STAT1, and STAT3 proteins in each group. Results In vivo, Guomin Decoction demonstrated significant therapeutic effects in a mouse model of AD. Compared with the Model group, Guomin Decoction intervention significantly reduced scratching behavior, ear swelling, and pathological changes in ear lesions. Additionally, the spleen index was downregulated, the thymic index was elevated, and the number of mast cells was reduced. Serum levels of TSLP, IL-4, IL-5, IL-33, IgE, HIS, and LTB4 were significantly decreased, as were IL-4, TNF-α, and IL-33 levels in skin lesion tissues. Cellular experiments further revealed that Guomin Decoction concentrations ranging from 23 to 750 μg/mL had no significant impact on RAW264.7 cell viability. The decoction notably suppressed NO and IL-6 production, as well as the phosphorylation of JAK1, JAK2, STAT1, and STAT3 proteins in the JAK/STAT pathway. Conclusion Guomin Decoction may alleviate the inflammatory response in AD by inhibiting the activation of the macrophage JAK1/JAK2-STAT1/STAT3 signaling pathway, highlighting its potential as a therapeutic agent for inflammatory skin diseases.