Hepatocyte protection and stellate cell control by Salvia miltiorrhiza in liver fibrosis

Salvia miltiorrhiza Bunge provides chemically distinct candidates for hepatocyte protection and hepatic stellate cell (HSC) control. This critical narrative Mini Review examines whether these effects occur with one defined intervention at compatible exposure. HSC control is distinguished as elimination, sustained deactivation after withdrawal or short-term state suppression. Same-study observations include hepatocyte protection with HSC state suppression and salvianolic acid A-induced apoptosis in PDGF-stimulated HSCs with preserved primary-hepatocyte viability. These findings provide partial support for cellular selectivity, but do not establish injured-hepatocyte rescue and HSC control within a pharmacologically supported exposure interval. Opposing ferroptosis effects among tanshinones further preclude class-level mechanistic inference. Clinical findings concern specific preparations and endpoints, and do not resolve the paired cellular question. Priorities are chemical and batch characterization, authenticated human models, validated fate endpoints, state- or subset-selectivity that preserves HSC homeostatic functions, and measurement of achieved exposure and target engagement. A useful window should meet separate hepatocyte-benefit, safety and HSC-control criteria, with donor-level effect estimates and confidence intervals. Distinguishing intrinsic susceptibility from delivery-mediated enrichment is essential for translating these candidates into reproducible antifibrotic interventions.