Investigating the molecular mechanism of purslane‑based vitiligo treatment using network pharmacology, molecular docking and in vitro analyses.

利用网络药理学、分子对接和体外分析研究马齿苋治疗白癜风的分子机制

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作者:Zhang Xueying, Meng Lele, Ran Xiaorong, Li Shuang, Wen Changhui
Purslane is a traditional Chinese medicine with a long‑standing history of efficacy in the management of dermatological conditions such as vitiligo. However, the molecular mechanisms underlying its therapeutic effects on vitiligo remain unclear. Therefore, the present study explored these mechanisms using network pharmacology, molecular docking and in vitro experiments. Following the screening process, seven principal active components were identified, namely kaempferol, hesperetin, luteolin, quercetin, arachidonic acid, cycloartenol and β‑sitosterol. In addition, six key targets, namely AKT1, tumor protein p53, peroxisome proliferator‑activated receptor γ (PPARG), estrogen receptor 1, prostaglandin‑endoperoxidase synthase 2 and mitogen‑activated protein kinase 1, and eight pathways in purslane‑based vitiligo treatment were identified. Network pharmacology and molecular docking demonstrated that flavonoids are the key components of purslane likely to mitigate oxidative stress damage in vitiligo. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the phosphatidylinositol 3‑kinase (PI3K)/AKT, p53 and PPARG signaling pathways are associated with purslane components and vitiligo. In vitro experiments revealed that purslane total flavones (PTF) increased cell viability, decreased ROS levels and increased antioxidant enzyme activities in H(2)O(2)‑induced B16F10 cells. In addition, PTF activated the PI3K/AKT signaling pathway in H(2)O(2)‑induced B16F10 cells, and the antioxidant effect of PTF was attenuated by a PI3K/AKT inhibitor. In conclusion, the findings of the present study suggest that the flavonoids of purslane contribute, at least in part, to its therapeutic effectiveness in vitiligo by mitigating oxidative stress in melanocytes through the PI3K/AKT signaling pathway.

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