AIM: To investigate the protective effect and mechanism of Guomin decoction on 1-chloro-2, 4-dinitrochlorobenzene (DNCB) induced atopic dermatitis (AD) in mice. METHODS: Fifty mice were induced by DNCB to establish atopic dermatitis model, and were randomly divided into model group, Cetirizine hydrochloride group (1.3 mg/kg), Guomin decoction low, medium and high-dose groups (3.25, 6.5, 13 g/kg), and blank group 10 mice, 60 mice in total. Each group of mice was given the corresponding test drug according to the set dose by intragastric administration for 14 consecutive days. The skin lesions were observed and the severity of skin lesions were scored. The organ index was calculated after treatment. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of skin lesions. Serum immunoglobulin E (Ig-E), interleukin-6 (IL-6), IL-1β, tumor necrosis factor alpha (TNF-ɑ), interferon gamma (IFN-γ) and transforming growth factor β (TGF-β) were detected by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative polymerase chain reaction (Real-Time) the gene expression of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear transcription factor κB (NF-κB), NF-κB inhibitory protein α (IκB-α) were detected by PCR. The expression levels of TLR4, MyD88, NF-κBp65 and p-NF-κBp65 in skin lesions were detected by Western Blot. RESULTS: Compared with blank group, the lesion score of mice in model group was increased (P<0.01). The epidermis was hyperkeratosis, the spinous layer was hypertrophic, and eosinophils and other inflammatory cells infiltrated the dermis. Spleen index and serum IgE, IL-6, IL-1β, TNF-alpha and IFN-γ were increased (P<0.01), while TGF-β1 was decreased (P<0.01). The expressions of TLR4, MyD88, NF-κB, NF-κBp65 and P-NF-κBP65 were increased, while the expressions of IκB-α were decreased, with statistical significance (P<0.01). Compared with the model group, the skin area of mice in the allergic decoction group was reduced and the score was decreased (P<0.01). The epidermal hyperkeratosis was alleviated, the spinous layer was slightly hypertrophic, and there was a small amount of inflammatory cell infiltration in the dermis. Spleen index and serum IgE, IL-6, IL-1β, TNF-alpha and IFN-γ were decreased (P<0.01), while TGF-β1 was increased (P<0.01). The expressions of TLR4, MyD88, NF-κB, NF-κBp65 and P-NF-κBP65 were decreased, while the expressions of IκB-α were increased (P<0.05). CONCLUSION: Guomin decoction can relieve pruritus, spleen index and skin inflammation in AD mice. It may regulate inflammatory response and transcription through TLR signaling pathway, inhibit the activation of p65 subunit in NF-κB, and affect the release of downstream inflammatory factors to achieve therapeutic effects.
