ArticleFrontiers in cell and developmental biology2026
Sodium alginate-based dual-responsive nanoparticles co-loaded with baicalin and doxorubicin induce ferroptosis in hepatocellular carcinoma associated with the PI3K/AKT/FoxO3α axis regulation.
Article in Frontiers in cell and developmental biology, 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
Background: Hepatocellular carcinoma (HCC) has high malignancy, poor prognosis, and frequent chemo-resistance. Doxorubicin (DOX) has strong anti-tumor activity but severe systemic toxicity; baicalin (BAI) acts against HCC yet has poor solubility and low bioavailability. Marine sodium alginate (SA) is a biocompatible carrier for responsive nanomedicines. We fabricated pH/GSH dual-responsive SA nanoparticles co-loaded with BAI and DOX (DOX/BAI NPs), tested synergistic anti-HCC activity, and verified the correlation between the PI3K/AKT/FOXO3α axis and DOX/BAI NPs-induced ferroptosis. Methods: Amphiphilic SA-SS-BAI was synthesized via cystamine disulfide bonds and self-assembled to encapsulate DOX. We characterized physicochemical traits, dual responsiveness, stability, and drug release. HepG2 cell uptake, endocytosis, and cytotoxicity were measured. Ferroptosis markers (ROS, Fe Results: SA-SS-BAI-4 formed uniform ∼148 nm spherical DOX/BAI NPs with good loading and encapsulation. NPs stayed stable physiologically and disassembled rapidly under low pH plus high GSH. Caveolae-dependent uptake was greatly boosted in HepG2 cells, yielding stronger growth inhibition than free drugs or physical mixtures. NPs triggered robust ferroptosis via ROS/Fe Conclusion: This dual pH/GSH-responsive SA DOX/BAI nanoplatform exerts synergistic anti-HCC effects by inducing ferroptosis, which is associated with PI3K/AKT/FOXO3α axis suppression. The marine polysaccharide carrier overcomes BAI and DOX solubility/toxicity defects, creates a practical HCC combinatorial nanotherapy, and defines a potential correlation between the PI3K/AKT/FOXO3α regulatory axis and hepatic cancer ferroptosis.
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