Objective To investigate the effect and mechanism of narrow-band ultraviolet B (NB-UVB) in promoting vitamin D (VD) metabolism and alleviating imiquimod (IMQ) induced psoriasis like dermatitis in mice. Method C57BL/6 mice were treated with IMQ cream on the back skin to induce psoriasis like dermatitis. The levels of VD metabolites 25(OH)D3 and 1,25(OH)2D3 in serum were detected, as well as the expression of VD receptor (VDR) mRNA in the skin lesions; After determining the irradiation energy of NB-UVB irradiated mice, the model group combined with NB-UVB irradiation was performed to observe mouse skin lesions. The levels of 25(OH)D3, 1,25(OH)2D3 in serum, VDR and inflammatory factors (IL-17A, IL-23, TNF-α、IL-1β) mRNA expression and inflammatory factors protein contents in skin lesions, and the proportion of CD3+ CD4+ IL-17A+ T cells were detected. After pretreatment with the specific inhibitor Dafadine-A to block CYP27A1 activity (cytochrome P450 family 27 subfamily A, polypeptide 1, a key enzyme in vitamin D metabolism), the mice underwent psoriasiform dermatitis induction followed by NB-UVB irradiation. Skin lesions were observed, the proportion of CD3+ CD4+ IL-17A+ T cells, inflammatory factors and VDR mRNA expression in the skin lesions, and serum levels of 25(OH)D3 and 1,25(OH)2D3 were detected. Results The levels of 25(OH)D3 and 1,25(OH)2D3 in the serum of psoriasis like mouse models and the mRNA expression of VDR in skin lesions were significantly reduced. After NB-UVB irradiation on a psoriasis like mouse model, compared to the model group, the levels of 25(OH)D3, 1,25(OH)2D3 in the serum of the irradiated mice and the mRNA expression of VDR in the skin lesions were upregulated. The mRNA expression and content of inflammatory factors in the skin lesions were downregulated, and the proportion of IL-17A secreting CD3+ CD4+ T cells was significantly reduced. Compared to the IMQ+NB-UVB group, Dafadine-A pretreated mice showed significantly decreased serum levels of 25(OH)D3 and 1,25(OH)2D3, reduced VDR mRNA expression in skin lesions, along with significantly increased proportions of CD3+ CD4+ IL-17A+ T cells and elevated inflammatory cytokine levels in lesions. Conclusion NB-UVB irradiation ameliorates psoriasiform dermatitis and cutaneous inflammation in mice by promoting vitamin D metabolic pathways. Importantly, specific inhibition of CYP27A1 markedly attenuates the therapeutic effects of NB-UVB on both psoriatic skin lesions and associated inflammatory responses.