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Life sciences · Journal article
Planta Medica · October 23, 2026
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Abstract Chenopodiastrum hybridum (CH) is an edible and folk medicinal plant, yet its efficacy and molecular mechanisms against ovarian cancer (OC) remain unclear, restricting its antitumor application. This study investigated the anti-OC effects and underlying mechanisms of CH via dose-effect weighted network pharmacology to provide experimental evidence for its clinical and medicinal development. This study determined the total flavonoid content of CH refined extract (CHRE) and assessed its inhibitory effect on OVCAR-3 cell proliferation. CHRE’s antioxidant and anti-inflammatory activities were evaluated by free-radical scavenging ability and detection of ROS, NO, TNF-α, and IL-6 levels. Network pharmacology, molecular docking, and molecular dynamics simulations were applied to screen core targets and key pathways, with RT-qPCR verifying target gene expression. Flavonoid-rich CHRE significantly inhibited OVCAR-3 cell growth, exhibiting potent antioxidant and anti-inflammatory activities. The estrogen signaling pathway was identified as the core regulatory pathway. CH’s key active compounds bound stably to the core targets (epidermal growth factor receptor [EGFR], ESR1, SRC, HSP90AA1, AKT1). RT-qPCR revealed downregulated mRNA levels of EGFR, AKT1, KDR, ESR1, and upregulated HSP90AA1 expression. CH suppresses OC proliferation by activating the estrogen signaling pathway to alleviate oxidative stress and inflammation. This study elucidates CH’s anti-OC mechanism, offering valuable references for developing novel natural botanical drugs and auxiliary clinical therapies for OC.