Scheme 1

Schematic illustration of the transportation and therapeutic mechanism of MLNPs against HCC. After oral administration, MLNPs maintained stability during their passage through the GIT and modulated intestinal microbiota. The superior property effectively facilitated their unimpeded transit from the GIT into the hepatic vasculature via systemic circulation, ensuring comprehensive liver targeting. Subsequently, MLNPs underwent cellular internalization by liver tumor cells through the galactose-mediated endocytic processes. This intricate internalization mechanism further facilitated the efficacious eradication of Hepa1-6 cells by heightening intracellular oxidative stress, provoking mitochondrial damage, and inducing cell cycle arrest