Hepatic fibrosis, for which no effective pharmacological interventions currently exist, is characterized by progressive scarring and architectural distortion. The pathogenesis involves excessive accumulation of extracellular matrix components, predominantly synthesized by activated hepatic stellate cells (HSCs). HSCs can be activated by inflammatory signals and injured hepatocytes, processes linked to intestinal microbiota dysbiosis. Therefore, HSCs and associated pathways constitute promising therapeutic targets for antifibrotic strategies. Recent evidence suggests that ginsenosides, principal bioactive constituents of Panax ginseng, demonstrate hepatoprotective and antifibrotic properties. Ginsenosides are structurally classified into dammarane-type, ocotillol-type, and oleanane-type saponins, showing favorable safety profiles. Their pharmacological activity is critically dependent on structural features, including the quantity, type, and glycosylation positions of sugar moieties, as well as the stereochemical configuration at the C-20 position. The antifibrotic mechanisms of ginsenosides encompass multiple pathways: suppression of HSC activation, induction of HSC death, amelioration of hepatocellular injury, attenuation of inflammatory responses, and modulation of intestinal microbiota composition. This review aims to evaluate ginsenosides as potential therapeutic agents for hepatic fibrosis and to establish a theoretical framework for their clinical translation in the management of this condition. Ginsenosides attenuate liver fibrosis via various mechanisms. Ginsenosides alleviate liver fibrosis via suppressing HSC activation, inducing HSC death, attenuating hepatocyte injury, inhibiting liver inflammation, and modulating intestinal microbiota.
Wu et al. (2026) studied this question.