Silymarin-Based Therapies in Chronic Liver Disease: A Systematic Review of Biochemical, Cardiometabolic, Steatosis, and Fibrosis-Related Outcomes
- 1Department of Internal Medicine, Hanyang University College of Medicine, Seoul 04763, Republic of Korea
- 2Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Republic of Korea
- 3Institute of Advanced BioConvergence, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul 04763, Republic of Korea
Abstract
Background/Objectives: Silymarin is a widely used hepatoprotective agent; however, its effects on hepatic steatosis and fibrosis remain unclear. We systematically reviewed the effects of silymarin on liver biochemical parameters, fibrosis, steatosis, and cardiometabolic outcomes, as well as its safety, in chronic liver disease. Methods: PubMed, Embase, and the Cochrane Library were searched from inception to June 11, 2026. Randomized controlled trials (RCTs) and eligible comparative clinical studies that evaluated the use of oral silymarin were included. Risk of bias was evaluated using RoB 2 for randomized trials and ROBINS-I for non-randomized studies. Random-effects meta-analyses were performed for alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in placebo-controlled RCTs of silymarin monotherapy and for liver stiffness measurement (LSM) in placebo-controlled RCTs, and the certainty of evidence was assessed using GRADE. Results: Forty-seven studies (37 RCTs and 10 non-randomized studies) met the inclusion criteria. Compared with placebo, silymarin monotherapy significantly reduced ALT (six trials; mean difference [MD], −7.25 IU/L; 95% confidence interval [CI], −11.60 to −2.89) and AST (four trials; MD, −5.36 IU/L; 95% CI, −8.45 to −2.27). In addition, an exploratory meta-analysis of three placebo-controlled RCTs showed a greater reduction in LSM with silymarin-based interventions than with placebo (MD, −0.60 kPa; 95% CI, −1.04 to −0.16). Conclusions: In placebo-controlled trials, silymarin monotherapy significantly reduced serum aminotransferase levels, and an exploratory meta-analysis of three trials also showed a reduction in liver stiffness with silymarin-based interventions. Silymarin was generally well tolerated. Well-designed long-term randomized controlled trials using validated noninvasive or histological fibrosis endpoints are warranted to determine whether these improvements translate into antifibrotic and clinically meaningful benefits.
Related
- Cardiometabolic Substrate Modification in Atrial Fibrillation: Obesity and Epicardial Adipose Tissue in the Era of Incretin-Based Therapies and Catheter Ablation
- Incretin‐Based Therapies as Cardiometabolic Interventions: Outcome Hierarchy, Receptor‐Network Pharmacology and Phenotype‐Based Clinical Positioning
- Contemporary cardiometabolic and inflammation targeting therapies reduce residual cardiovascular risk in an endpoint harmonized meta analysis
- GLP-1-Based therapies for obesity-related heart failure with preserved ejection fraction: an umbrella review incorporating broader heart failure and cardiometabolic evidence
- Beyond BMI: The Role of Visceral Adipose Tissue in Cardiometabolic Risk Stratification Among Children and Adolescents with Obesity—A Systematic Review
BibTeX
@article{lee2026silymarinbased,
title = {{Silymarin-Based Therapies in Chronic Liver Disease: A Systematic Review of Biochemical, Cardiometabolic, Steatosis, and Fibrosis-Related Outcomes}},
author = {Hyo Young Lee and Hyunwoo Oh and Eileen Laurel Yoon and Dae Won Jun},
journal = {Nutrients},
year = {2026},
month = nov,
doi = {10.3390/nu18213685},
url = {https://www.mdpi.com/2072-6643/18/21/3685},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Silymarin-Based Therapies in Chronic Liver Disease: A Systematic Review of Biochemical, Cardiometabolic, Steatosis, and Fibrosis-Related Outcomes
AU - Hyo Young Lee
AU - Hyunwoo Oh
AU - Eileen Laurel Yoon
AU - Dae Won Jun
PY - 2026
DA - 2026/11/06
JO - Nutrients
DO - 10.3390/nu18213685
UR - https://www.mdpi.com/2072-6643/18/21/3685
AB - Background/Objectives: Silymarin is a widely used hepatoprotective agent; however, its effects on hepatic steatosis and fibrosis remain unclear. We systematically reviewed the effects of silymarin on liver biochemical parameters, fibrosis, steatosis, and cardiometabolic outcomes, as well as its safety, in chronic liver disease. Methods: PubMed, Embase, and the Cochrane Library were searched from inception to June 11, 2026. Randomized controlled trials (RCTs) and eligible comparative clinical studies that evaluated the use of oral silymarin were included. Risk of bias was evaluated using RoB 2 for randomized trials and ROBINS-I for non-randomized studies. Random-effects meta-analyses were performed for alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in placebo-controlled RCTs of silymarin monotherapy and for liver stiffness measurement (LSM) in placebo-controlled RCTs, and the certainty of evidence was assessed using GRADE. Results: Forty-seven studies (37 RCTs and 10 non-randomized studies) met the inclusion criteria. Compared with placebo, silymarin monotherapy significantly reduced ALT (six trials; mean difference [MD], −7.25 IU/L; 95% confidence interval [CI], −11.60 to −2.89) and AST (four trials; MD, −5.36 IU/L; 95% CI, −8.45 to −2.27). In addition, an exploratory meta-analysis of three placebo-controlled RCTs showed a greater reduction in LSM with silymarin-based interventions than with placebo (MD, −0.60 kPa; 95% CI, −1.04 to −0.16). Conclusions: In placebo-controlled trials, silymarin monotherapy significantly reduced serum aminotransferase levels, and an exploratory meta-analysis of three trials also showed a reduction in liver stiffness with silymarin-based interventions. Silymarin was generally well tolerated. Well-designed long-term randomized controlled trials using validated noninvasive or histological fibrosis endpoints are warranted to determine whether these improvements translate into antifibrotic and clinically meaningful benefits.
SN - 2072-6643
ER -