Hepatoprotective effects and mechanistic basis of cinnamaldehyde in preclinical liver disease models: A systematic review.
- 2026-05
- The Journal of international medical research 54(5)
- Jueliang Li
- Wei Chen
- Qianhui Lai
- Honglei Zhao
- PubMed: 42130112
- DOI: 10.1177/03000605261447143
Study Design
- Type
- Systematic Review
- Methods
- A systematic search was conducted in PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure, and Wanfang databases from inception through January 2026. Studies were considered eligible if cinnamaldehyde was used as the main intervention in liver-related disease or injury models and reported at least one liver-relevant outcome. Data extraction and study selection were performed independently by two reviewers. Risk of bias was assessed using RoB 2.0.
ObjectiveTo systematically evaluate the preclinical evidence on the hepatoprotective effects of cinnamaldehyde and summarize the key biological mechanisms underlying its actions across different liver disease settings.MethodsA systematic search was conducted in PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure, and Wanfang databases from inception through January 2026. Studies were considered eligible if cinnamaldehyde was used as the main intervention in liver-related disease or injury models and reported at least one liver-relevant outcome was reported. Data extraction and study selection were performed independently by two reviewers. Risk of bias was assessed using RoB 2.0.ResultsA total of 454 records were identified, of which 9 studies met the eligibility criteria for qualitative synthesis. All included studies were preclinical, comprising in vivo, in vitro, or combined designs. The evidence covered liver fibrosis, metabolic liver injury or steatosis, infection-associated liver injury, and hepatic encephalopathy. Across these settings, cinnamaldehyde was consistently associated with improved liver biochemical indices, attenuation of histopathological injury, and reductions in steatosis, collagen deposition, inflammation, oxidative stress, and apoptosis. Mechanistically, the reported effects involved several pathways associated with fibrogenesis, metabolic regulation, inflammatory signaling, and liver-brain axis dysfunction.ConclusionCurrent preclinical evidence supports the use of cinnamaldehyde as a promising hepatoprotective compound with multitarget activity across several liver injury contexts. However, the available data remain limited to experimental studies; therefore, further studies are warranted to clarify its pharmacological profile, cell-specific mechanisms, and translational relevance.Registration: The protocol was registered with the International Prospective Register of Systematic Reviews database (CRD420261346515).