ArticleBMC complementary medicine and therapies2026
An integrated strategy for screening Q-markers and elucidating anti-fibrotic mechanisms of Ganoderma lucidum.
Article in BMC complementary medicine and therapies, 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
backgroundGanoderma lucidum (G. lucidum) is a medicinal mushroom known for its hepatoprotective effects against various liver diseases.
objectiveAddressing the variable quality of G. lucidum samples and the lack of efficacy-linked quality control criteria, an integrated strategy combining chemical analysis and biological validation was conducted to identify the Q-markers directly responsible for its anti-hepatic fibrosis (HF) activity and to preliminarily elucidate their action mechanism.
methods49 batches of G. lucidum samples were collected from 15 geographical origins across 7 provinces in China. Initially, UPLC fingerprinting integrated with chemometric analysis evaluated the quality and identified differential chemical components. The common compounds were further characterized by UPLC-Orbitrap-HRMS. Subsequently, the potential targets and binding affinity were predicted by network pharmacology and molecular docking. Finally, the anti-HF activity and underlying mechanism of the core Q-marker were verified in a TGF-β1-induced HSC-T6 model using CCK-8, flow cytometry, immunofluorescence, and Western blotting.
resultsThe UPLC chemical fingerprint of G. lucidum was successfully established, 49 common components were identified based on UPLC-Orbitrap-HRMS analysis, mostly were triterpenoids. Through chemometric analysis, 19 key differential markers were subsequently screened. Then, by integrating network pharmacology predictions with chemometric screening results, 7 triterpenoids were ultimately determined as potential Q-markers for the anti-HF activity of G. lucidum. Ganoderic acid J (GAJ) demonstrated robust binding specificity to pivotal targets within the PI3K/AKT signaling pathway through molecular docking. 5, 10, and 20 µg/mL at 24 h were confirmed as low, medium, and high doses of GAJ by CCK-8, respectively. Ultimately, HF was relieved by suppressing the PI3K/AKT pathway, promoting apoptosis in activated HSCs and normalizing the MMP1/MMP2 equilibrium.
conclusionThe anti-HF effects of G. lucidum were mediated through multi-target synergistic actions, chiefly by suppressing the PI3K/AKT pathway and modulating extracellular matrix metabolism. The hepatoprotective mechanism of G. lucidum was elucidated at the molecular level, and a Q-marker-based theoretical framework was established for quality control of traditional medicines and innovative drug development.
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