Background
Propofol, commonly used as an intravenous anesthetic during pregnancy, can easily penetrate the placental barrier, potentially affecting fetal heart development. This study aims to investigate propofol's impact on developing zebrafish heart structure and function, and identify potential drug targets.
Conclusion
In conclusion, our study indicates that propofol alters the structure and function of the developing zebrafish heart, with the mitochondrial-related gene agxt2 possibly being a target of its pharmacological effects.
Methods
Zebrafish embryos were exposed to different concentrations of propofol (0.5, 1, and 5 mg/L) to observe changes in zebrafish larval heart structure and function (heart rate). In vitro cell experiments were conducted to assess the effects of propofol at different concentrations on cardiomyocyte viability and migration. Transcriptomic sequencing was utilized to identify and validate potential drug targets associated with propofol-induced cardiac toxicity.
Results
The results demonstrate that propofol dose-dependently reduces the hatching and survival rates of zebrafish larvae, while increasing the rate of deformities. Transgenic green fluorescent zebrafish larvae exposed to propofol exhibit enlarged cardiac cavities, and HE staining reveals thinning of the myocardial wall. Additionally, propofol-treated zebrafish larvae show a decrease in heart rate. We also assess the impact of propofol on myocardial cell function, showing decreased cell viability, reduced migration function, and increased apoptosis. Finally, transcriptome sequencing analysis and differential gene co-expression network analysis identify agxt2 as a potential target of propofol-induced cardiac toxicity.