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Ginsenoside Rk3 exerts the strong activity inhibiting NF-κB in a dose-dependent manner. HepG2 cells are pre-treated with different ginsenosides at concentrations ranging from 0.01 to 10 μM for 1 h, and induced with TNF-α for 20 h. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC ₅₀ of 14.24±1.30 μM. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC ₅₀ of 15.32±0.29 μM in SK-Hep1 cells, consistent with the data from HepG2 cells. Consistent with the inhibition of NF-κB, Ginsenoside Rk3 inhibits the induction of IL8 , CXCL1 , iNOS , and ICAM1 mRNA significantly in a dose-dependent manner.

The inhibitory effects of Ginsenoside Rk3 (Rk3) on tumor progression are studied in vivo using a H460 xenograft model in nude mice. Compared with the control group, a significant inhibition of tumor growth (volume) is observed in the Ginsenoside Rk3-treated group. Twenty-one days after treatment initiation, tumor growth is significantly inhibited by approximately 62.99% in the mice receiving 20 mg/kg Ginsenoside Rk3, similar to the inhibitory effect observed in the 20 mg/kg Gefitinib-treated group (57.21%). Compared with the control group, tumor growth is moderately inhibited in the mice receiving 10 and 5 mg/kg Ginsenoside Rk3, with inhibition rates of 32.54% and 11.84%, respectively.