Document Type : Review Article
Authors
1
Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran
2
Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran
3
Department of Physiology, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran
Abstract
Objective: Hepatotoxicity induced by pharmaceuticals, environmental toxins, and industrial chemicals represents a critical public health concern, necessitating effective protective strategies. This systematic review evaluates the hepatoprotective efficacy of zerumbone, a bioactive compound derived from Zingiber zerumbet L., against drug-induced liver injury through comprehensive analysis of experimental and preclinical studies.
Materials and Methods: Following PRISMA guidelines, the literature search was done across PubMed, Scopus, Web of Science, and Google Scholar focusing on studies examining zerumbone effects on biochemical markers, oxidative stress, and histopathological outcomes. The search strategy employed MeSH terms up to January 2025.
Results: Key findings demonstrate zerumbone multifaceted mechanisms: 1- Antioxidant activity through reactive oxygen species (ROS) reduction vs. controls, superoxide dismutase (SOD)/catalase (CAT) activities enhancement, and lipid peroxidation (MDA) inhibition. 2- Anti-apoptotic effects via caspase-3 suppression and Bcl-2 upregulation, as well as preserving hepatocyte viability. 3- Anti-inflammatory action by nuclear factor kappa B )NF-κB( inhibition, reducing tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2) and 5-Lipoxygenase (5-LOX) suppression. 4- Functional recovery evidenced by normalized liver enzymes aspartate transaminase (AST) and alanine aminotransferase (ALT) as well as reduction of bilirubin levels. Notably, zerumbone showed dose-dependent efficacy across diverse hepatotoxicants (paracetamol, carbon tetrachloride (CCl₄), and cisplatin).
Conclusion: These findings underscore zerumbone translational potential in managing drug-induced hepatotoxicity while highlighting critical research gaps that need to be addressed for clinical implementation.
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