Toosendanin triggered hepatotoxicity in zebrafish via inflammation, autophagy, and apoptosis pathways

Toosendanin (TSN) is a crucial component from Toosendan Fructus with a promising anti-tumor capacity. It is also the primary suspect hepatotoxic component of Toosendan Fructus. However, the mechanisms underlying TSN-induced liver injury are still largely unknown. In present study, we evaluated the h...

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Veröffentlicht in:Comparative biochemistry and physiology. Toxicology & pharmacology 2021-12, Vol.250, p.109171, Article 109171
Hauptverfasser: Sun, Meng, Liu, Qing, Liang, Qiuxia, Gao, Shuo, Zhuang, Kaiyan, Zhang, Yun, Zhang, Huazheng, Liu, Kechun, She, Gaimei, Xia, Qing
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Sprache:eng
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Zusammenfassung:Toosendanin (TSN) is a crucial component from Toosendan Fructus with a promising anti-tumor capacity. It is also the primary suspect hepatotoxic component of Toosendan Fructus. However, the mechanisms underlying TSN-induced liver injury are still largely unknown. In present study, we evaluated the hepatotoxicity of TSN on zebrafish and explored the role of inflammation, autophagy, and apoptosis in TSN-induced hepatotoxicity. We found that TSN treatment decreased the area and fluorescence intensity of zebrafish liver in time- and dose-dependent manners at nonlethal concentrations. The ALT and AST activities were increased after TSN treatment. Severe cytoplasmic vacuolation and nuclear shrank were found in the liver of TSN-treated zebrafish. The expression profile of genes demonstrated that inflammation, autophagy and apoptosis pathways were involved in TSN-induced hepatotoxicity. Our study demonstrated for the first time that TSN treatment gave rise to liver injury in zebrafish, and inflammation, autophagy, apoptosis played a role in TSN-induced hepatotoxicity. [Display omitted] •TSN treatment decreased the area and fluorescence intensity of zebrafish liver.•Cytoplasmic vacuolation and nuclear shrank occurred in TSN-treated zebrafish liver.•Inflammation, autophagy, and apoptosis played a role in TSN-induced hepatotoxicity.
ISSN:1532-0456
1878-1659
DOI:10.1016/j.cbpc.2021.109171