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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

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

  • Yifan Liu1,2
  • Wei Li3
  • Weiwei Wu4
  • Zihao Xu1,2
  • Deng Wu5,6,7,8
8 affiliations
  1. 1Hubei University of Chinese Medicine
  2. 2Hubei Province International Science and Technology Cooperation Base for Innovative Research and Development of Food and Drug Resources and Targeted Delivery
  3. 3Wuhan No.7 Hospital
  4. 4Zengdu District People’s Hospital of Suizhou City
  5. 5Hubei Key Laboratory of Theoretical and Applied Research of Liver and Kidney in Traditional Chinese Medicine, Hubei Provincial Hospital of Traditional Chinese Medicine, Institute of Liver Diseases
  6. 6Hubei Provincial Clinical Research Center of Traditional Chinese Medicine for Liver Diseases
  7. 7Hubei Shizhen Laboratory
  8. 8Affiliated Hospital of Hubei University of Chinese Medicine
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{liu2026hepatocyte,
  title = {{Hepatocyte protection and stellate cell control by Salvia miltiorrhiza in liver fibrosis}},
  author = {Yifan Liu and Wei Li and Weiwei Wu and Zihao Xu and Deng Wu},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.2006283},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.2006283/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Hepatocyte protection and stellate cell control by Salvia miltiorrhiza in liver fibrosis
AU  - Yifan Liu
AU  - Wei Li
AU  - Weiwei Wu
AU  - Zihao Xu
AU  - Deng Wu
PY  - 2026
DA  - 2026/10/26
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.2006283
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.2006283/full
AB  - 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.
SN  - 1663-9812
ER  -