Dual targeting by Artemisia rupestris L. disrupting TLR4/NF-κB signaling and macrophage driven immune evasion in hepatocellular carcinoma

ARL suppresses HCC progression by dual mechanisms that include the interference in TLR4/MyD88/NF-κB cascade to reduce proinflammatory cytokine production, and reprogramming macrophage polarization to attenuate immune driven tumor growth. These findings make ARL a promising natural therapeutic agent and provide an experimental basis for further in-depth subsequent exploration of the application of ARL in hepatocellular carcinoma.