Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
J Appl Toxicol. 2020 Nov;40(11):1491-1497. doi: 10.1002/jat.4000. Epub 2020 Jul 3.
The cardiotoxicity of cantharidin has been well characterized, but the understanding of the underlying mechanism(s) is incomplete. To more fully understand the differentially expressed genes (DEGs) in cantharidin-induced myocardial injury, Sprague-Dawley rats were exposed to cantharidin (1.34 mg/kg or 2.67 mg/kg) for 24 h and then the heart was sampled for pathologic changes analysis and RNA-sequencing-based transcriptomic profiling. In addition, serum troponin T (TN-T) levels were also tested using the enzyme-linked immunosorbent assay method. The results showed that cantharidin could cause myocardial damage and elevated serum TN-T levels. The genes with a fold change ≥2 were considered as DEGs and we found 38 DEGs that were mainly enriched in eight pathways revealed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The cellular component of gene ontology analysis showed that the DEGs were mostly enriched in the extracellular matrix. In conclusion, our present study demonstrated that cantharidin induces myocardial injury by multiple modulatory mechanisms, which provide new insights for further study of the pathophysiologic mechanism of cantharidin-induced myocardial injury.
斑蝥素的心脏毒性已得到充分证实，但对其潜在机制的理解尚不完全。为了更全面地了解斑蝥素诱导心肌损伤中的差异表达基因（DEGs），将 Sprague-Dawley 大鼠暴露于斑蝥素（1.34 mg/kg 或 2.67 mg/kg）24 小时后，取样进行病理变化分析和基于 RNA 测序的转录组分析。此外，还使用酶联免疫吸附测定法检测血清肌钙蛋白 T（TN-T）水平。结果表明，斑蝥素可引起心肌损伤和血清 TN-T 水平升高。倍数变化≥2 的基因被认为是 DEGs，我们发现了 38 个 DEGs，这些基因主要富集在京都基因与基因组百科全书（KEGG）通路分析揭示的 8 条通路中。基因本体论分析的细胞成分表明，DEGs 主要富集在细胞外基质中。总之，本研究表明斑蝥素通过多种调节机制诱导心肌损伤，为进一步研究斑蝥素诱导心肌损伤的病理生理机制提供了新的见解。
