Journal of inflammation research · 2025
Exploring the Mechanism of Qinzhuliangxue Mixture for Treating Skin Lesions in Atopic Dermatitis: Insights from Network Pharmacology and Experimental Validation.
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Qiao Yunxiao, Yin Hao, Zhang Haitang, He Qingyi, Li Yuting, Sun Lu, Wang Jie, Li Xiang, Koh Wan Xin, Pottakorn Aruncharoenphonchai, Chu Zewen, Xiang Yanwei
Аннотация
BACKGROUND: Atopic dermatitis (AD) is a chronic, recurrent inflammatory skin disorder that causes systemic skin lesions. The hospital preparation-Qinzhuliangxue mixture (QZLX) has shown potential in alleviating skin lesions in AD patients; however, its underlying mechanisms remain largely unexplored.
METHODS: QZLX's key compounds and their targets in AD skin lesions were screened by network pharmacology, and gene enrichment analysis was performed. Mouse model of AD induced by 2,4-dinitrofluorobenzene (DNFB) was established. Then animals were divided into control (Con), model (Model), dexamethasone (DSMS), and QZLX group. The DSMS group and QZLX group was orally administrated DSMS (10 mg/kg/day) and QZLX (18.27 g/kg/day) for 14 days respectively, after the DNFB was first injected intradermally into the abdomen of mice. Phenotypic changes in mice after treatment were evaluated by skin SCORAD score, hematoxylin-eosin (HE) staining, ELISA assays, and Western Blot (WB).
RESULTS: According to the findings of enrichment analysis based on GO and KEGG, QZLX may exert its effects at the top position via the JAK-STAT pathway. Subsequently the experimental validation showed that the skin score and HE staining of the QZLX group was significantly improved compared to the Model group (P < 0.05). Moreover, the levels of serum IgE, TSLP, and IL-4 in the QZLX group were notably lower than those in the Model group (P < 0.05). Furthermore, the expression of P-JAK2 and P-STAT3 detected by WB in the skin of the QZLX group was obviously higher than that in the Model group (P < 0.05).
CONCLUSION: QZLX demonstrated a significant ability to mitigate AD-like skin lesions and effectively reduced serum levels of IgE, TSLP, and IL-4 in AD mice. The underlying mechanism of action may involve modulation via the JAK2/STAT3 pathway.
METHODS: QZLX's key compounds and their targets in AD skin lesions were screened by network pharmacology, and gene enrichment analysis was performed. Mouse model of AD induced by 2,4-dinitrofluorobenzene (DNFB) was established. Then animals were divided into control (Con), model (Model), dexamethasone (DSMS), and QZLX group. The DSMS group and QZLX group was orally administrated DSMS (10 mg/kg/day) and QZLX (18.27 g/kg/day) for 14 days respectively, after the DNFB was first injected intradermally into the abdomen of mice. Phenotypic changes in mice after treatment were evaluated by skin SCORAD score, hematoxylin-eosin (HE) staining, ELISA assays, and Western Blot (WB).
RESULTS: According to the findings of enrichment analysis based on GO and KEGG, QZLX may exert its effects at the top position via the JAK-STAT pathway. Subsequently the experimental validation showed that the skin score and HE staining of the QZLX group was significantly improved compared to the Model group (P < 0.05). Moreover, the levels of serum IgE, TSLP, and IL-4 in the QZLX group were notably lower than those in the Model group (P < 0.05). Furthermore, the expression of P-JAK2 and P-STAT3 detected by WB in the skin of the QZLX group was obviously higher than that in the Model group (P < 0.05).
CONCLUSION: QZLX demonstrated a significant ability to mitigate AD-like skin lesions and effectively reduced serum levels of IgE, TSLP, and IL-4 in AD mice. The underlying mechanism of action may involve modulation via the JAK2/STAT3 pathway.