Exploring the Mechanism of Qinzhuliangxue Mixture for Treating Skin Lesions in Atopic Dermatitis: Insights from Network Pharmacology and Experimental Validation

Yunxiao Qiao,1,&ast; Hao Yin,2,3,&ast; Haitang Zhang,3 Qingyi He,4,5 Yuting Li,1 Lu Sun,6 Jie Wang,7 Xiang Li,1 Wan Xin Koh,1 Aruncharoenphonchai Pottakorn,1 Zewen Chu,4,5,&ast; Yanwei Xiang1,4,5,&ast; 1Yueyang Hospital of Integrative Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 2Institute of Vascular Disease, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 3Shanghai Integrated Traditional Chinese and Western Medicine Hospital, Shanghai, People’s Republic of China; 4School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 5Institute of Rehabilitation Medicine, Shanghai Academy of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 6The Second Rehabilitation Hospital of Shanghai, Shanghai, People’s Republic of China; 7Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Yanwei Xiang, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Pudong New Area, Shanghai, People’s Republic of China, Email [email protected] Zewen Chu, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Pudong New Area, Shanghai, People’s Republic of China, Email [email protected]: 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.Keywords: qinzhuliangxue mixture, atopic dermatitis, skin lesions, network pharmacology, molecular docking, JAK2/STAT3 pathway