Icaritin-Loaded Liposomes Mediated by Hyaluronic Acid Promoted the Anti-Proliferation and Senescence in Huh7 Cells
Icaritin (ICT) shows great potential in cancer therapy. To enhance the cancer-fighting properties of icaritin against hepatocellular carcinoma (HCC), we developed icaritin-loaded liposomes modified with hyaluronic acid (HA-Lip-ICT). We employed statistical design methods to analyze how various factors affected particle dimensions and drug encapsulation, creating an optimized HA-Lip-ICT formulation that could effectively suppress HCC cell growth and trigger cellular aging. The human HCC cell line Huh7 was then exposed to different icaritin preparations. We assessed tumor cell viability through multiple assays, including colony formation and DNA synthesis measurements. Our results demonstrated that the refined HA-Lip-ICT significantly impaired HCC cell proliferation. Moreover, at a concentration of 10 μmol/L, HA-Lip-ICT markedly accelerated cellular senescence in HCC cells. These observations support our initial hypothesis that HA-Lip-ICT can inhibit HCC cell growth and promote their aging. While further research is needed to elucidate the exact mechanisms, this approach shows the promise of HA-Lip-ICT as a targeted therapy for improving the HCC treatments.
Icaritin (ICT) shows great potential in cancer therapy. To enhance the cancer-fighting properties of icaritin against hepatocellular carcinoma (HCC), we developed icaritin-loaded liposomes modified with hyaluronic acid (HA-Lip-ICT). We employed statistical design methods to analyze how various factors affected particle dimensions and drug encapsulation, creating an optimized HA-Lip-ICT formulation that could effectively suppress HCC cell growth and trigger cellular aging. The human HCC cell line Huh7 was then exposed to different icaritin preparations. We assessed tumor cell viability through multiple assays, including colony formation and DNA synthesis measurements. Our results demonstrated that the refined HA-Lip-ICT significantly impaired HCC cell proliferation. Moreover, at a concentration of 10 μmol/L, HA-Lip-ICT markedly accelerated cellular senescence in HCC cells. These observations support our initial hypothesis that HA-Lip-ICT can inhibit HCC cell growth and promote their aging. While further research is needed to elucidate the exact mechanisms, this approach shows the promise of HA-Lip-ICT as a targeted therapy for improving the HCC treatments.
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