斑马鱼
自噬
细胞凋亡
炎症
肝损伤
细胞生物学
化学
癌症研究
生物
药理学
免疫学
生物化学
基因
作者
Meng Sun,Qing Liu,Qiuxia Liang,Shuo Gao,Kaiyan Zhuang,Yun Zhang,Huazheng Zhang,Kechun Liu,Gaimei She,Qing Xia
标识
DOI:10.1016/j.cbpc.2021.109171
摘要
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.
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