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November 21, 2025Frontiers in PharmacologyOpen Access

Epimedium brevicornu Maxim. extract activates natural killer cells against hepatocellular carcinoma via the cGAS-STING pathway

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Authors

LLLu LiuXZXiaoyan ZhanXWXianling Wang

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Overview

Laboratory experiments demonstrate tumor growth inhibition in hepatocellular carcinoma by activating natural killer cells through the cGAS-STING pathway.

Key Points

  • This research investigates the role of Epimedium brevicornu extract in activating natural killer cells to combat hepatocellular carcinoma.
  • Used ELISA and flow cytometry to assess NK cell activity.
  • Constructed co-culture model of NK-92 and K562 cells to evaluate NK cytotoxicity.
  • Employed murine HCC subcutaneous xenograft model to demonstrate in vivo effects of EPE on NK cell activation.
  • Conducted NK1.1 cell depletion experiments to confirm NK cell-dependent mechanisms.
  • Applied Western blotting and drug affinity responsive target stability assay to elucidate molecular mechanisms.
  • EPE enhanced cytokine release (IFN-γ, Granzyme B) in NK cells.
  • EPE increased activation markers (NKG2D, CD16) on NK cells.
  • Murine model showed EPE significantly reduced tumor growth and promoted cell death.
  • Depletion of NK1.1 cells reduced the anti-tumor effects of EPE.
  • Mechanistic studies identified EPE activation of the cGAS-STING pathway in NK cells.

Cite This Study

Liu et al. (2025) studied this question.

synapsesocial.com/papers/6924e405c0ce034ddc34f81chttps://doi.org/10.3389/fphar.2025.1681650
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