ArticleZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences2026
[Network pharmacology-based investigation of the therapeutic efficacy and molecular targets of Xiangsha Liujunzi decoction in thyroid carcinoma].
Article in Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo explore the active components and potential molecular mechanisms of Chinese medicine Xiangsha Liujunzi decoction (XSLJZ) in the treatment of thyroid carcinoma.
methodsActive components and corresponding targets of XSLJZ were screened using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). Thyroid cancer-related targets were collected from seven bioinformatics databases, including GeneCards, Online Mendelian Inheritance in Man Database (OMIM), DISGENET, DrugBank, The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Therapeutic Target Database (TTD). A protein-protein interaction (PPI) network and a multi-level "XSLJZ-medicinal materials-active components-potential targets-thyroid carcinoma" network were constructed to identify core targets. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed, followed by molecular docking to assess binding affinities.
resultsFive major active components of XSLJZ (isoliquiritigenin, naringenin, baicalein, nobiletin, and glycyrrhetinic acid) and 45 core targets for thyroid carcinoma were identified. XSLJZ and these five components significantly inhibited the proliferation of 8505C and TPC1 cells without notable toxicity to normal thyroid cells, with isoliquiritigenin showing the most prominent effect. Flow cytometry revealed that XSLJZ (16 mg/mL) induced up to (84.91±0.49)% death in TPC1 cells. Molecular docking showed low binding energies between isoliquiritigenin and protein kinase B 1 (Akt1), cysteine aspartic acid specific protease (Caspase)-3, Caspase-9, and poly ADP-ribose polymerase (PARP) (lowest －9.9 kcal/mol with PARP). XSLJZ and isoliquiritigenin dose-dependently suppressed colony formation and migration, downregu-lated receptor for advanced glycation end product (RAGE), phosphorylated phosphoino-sitide 3-kinase (PI3K), and phosphorylated Akt, upregulated B-cell lymphoma protein 2 associated X protein (BAX) and mitochondrial cytochrome c, and activated Caspase-3/9-mediated apoptosis and gasdermin E (GSDME)-dependent pyroptosis via the advanced glycation end product (AGE)-RAGE→PI3K/Akt axis.
conclusionsXSLJZ inhibits thyroid carcinoma cell proliferation and induces cell death through multi-component, multi-target synergistic regulation of the AGE-RAGE→PI3K/Akt signaling pathway.
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