Network Pharmacology and Molecular Docking Reveals Mechanism of Camphor on Liver Toxicity in Zebrafish

ABSTRACT

Objective
This study aimed to investigate the hepatotoxicity of camphor on zebrafish and its mechanism of toxicity.


Methods
We calculated concentration‐response curves for zebrafish larvae treated with camphor at 72‐h postexposure (hpe) and observed its toxic effects on liver. Employing network pharmacology and molecular pairs to predict key targets of camphor‐induced hepatotoxicity, these critical targets were subsequently validated via qPCR.


Results
This study indicates that following 72 hpe to camphor, the LC50 and LC10 values for zebrafish larvae were 336 and 300 μg/mL, respectively. Concentrations of 300‐ and 150‐μg/mL camphor significantly reduced liver fluorescence intensity and markedly elevated ALT and AST levels in zebrafish. At 300 μg/mL, pathological alterations in liver tissue were observed, including vacuolation, disordered hepatocyte arrangement and loosening of tissue structure, indicating potential hepatic damage. Integrative analysis via network pharmacology, molecular docking and qPCR revealed that camphor induces hepatotoxicity through multiple targets and pathways, either directly or indirectly. Key targets included GSR, GCLC and NQO1, while major involved pathways encompassed drug metabolism—other enzymes, chemical carcinogenesis—receptor activation, biosynthesis of cofactors and glutathione metabolism.


Conclusion
This study has identified potential hepatotoxicity of camphor in zebrafish larvae, with its toxic mechanism involving multiple targets and pathways. The primary targets are likely GSR, GCLC and NQO1.