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
Yueyang Hospital of Integrative Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Institute of Vascular Disease, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
J Inflamm Res. 2025 Apr 16;18:5173-5187. doi: 10.2147/JIR.S509607. eCollection 2025.
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.
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).
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).
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.
特应性皮炎（AD）是一种慢性复发性炎症性皮肤病，可导致全身性皮肤病变。医院制剂——芩珠凉血合剂（QZLX）已显示出减轻AD患者皮肤病变的潜力；然而，其潜在机制在很大程度上仍未得到探索。
通过网络药理学筛选QZLX在AD皮肤病变中的关键化合物及其靶点，并进行基因富集分析。建立2,4-二硝基氟苯（DNFB）诱导的AD小鼠模型。然后将动物分为对照组（Con）、模型组（Model）、地塞米松（DSMS）组和QZLX组。在首次将DNFB皮内注射到小鼠腹部后，DSMS组和QZLX组分别口服给予地塞米松（10mg/kg/天）和QZLX（18.27g/kg/天），持续14天。通过皮肤SCORAD评分、苏木精-伊红（HE）染色、酶联免疫吸附测定（ELISA）和蛋白质免疫印迹法（WB）评估治疗后小鼠的表型变化。
根据基于基因本体论（GO）和京都基因与基因组百科全书（KEGG）的富集分析结果，QZLX可能通过JAK-STAT途径在首位发挥作用。随后的实验验证表明，与模型组相比，QZLX组的皮肤评分和HE染色有显著改善（P<0.05）。此外，QZLX组血清IgE、胸腺基质淋巴细胞生成素（TSLP）和白细胞介素-4（IL-4）水平明显低于模型组（P<0.05）。此外，WB检测到QZLX组皮肤中磷酸化JAK2（P-JAK2）和磷酸化信号转导和转录激活因子3（P-STAT3）的表达明显高于模型组（P<0.05）。
QZLX显示出显著减轻AD样皮肤病变的能力，并有效降低AD小鼠血清中IgE、TSLP和IL-4水平。其潜在作用机制可能涉及通过JAK2/STAT3途径进行调节。
