Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide
Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide
复制标题
DOI：
10.1038/s41598-020-58739-4
复制
发表时间：
2020-02-12
影响因子：
4.6
通讯作者：
Taniguchi, Hideki
中科院分区：
文献类型：
--
作者：
Matsuo, Megumi;Murata, Soichiro;Taniguchi, Hideki
虽然肝移植是肝硬化唯一的确定性治疗方法，但供体仍然短缺，需要开发新的治疗方法。我们的目的是建立一个食蟹猴肝纤维化模型，可以帮助加快临床前研究。硫代乙酰胺（TAA）和四氯化碳（CCl 4）诱导肝纤维化。残余肝功能和纤维化进展的分析是基于临床指标，如Child-Pugh评分或纤维化标志物，除了组织学。TAA诱导明显的纤维化，而CCl 4不诱导纤维化。残余肝功能方面，TAA和CCl 4均使Child-Pugh评分指数恶化，但只有TAA模型增加了吲哚菁绿色的保留率。食蟹猴中TAA诱导的纤维化模型显示纤维化和残余肝功能，模拟Child-Pugh分级B。鉴于我们的模型是由临床指标评估的，它可以适用于临床前研究。
Although transplantation is the only definitive treatment for liver cirrhosis, there remains a shortage of donors, necessitating that novel treatments be developed. We aimed to establish a liver fibrosis model in Macaca fascicularis that can help accelerate preclinical research. Liver fibrosis was induced by administering thioacetamide (TAA) and carbon tetrachloride (CCl4). Analysis of residual liver function and fibrosis progression was based on clinical indices, such as the Child-Pugh score or fibrotic markers, besides histology. TAA-induced marked fibrosis, whereas CCl4 did not induce fibrosis. Concerning residual liver function, both of TAA and CCl4 worsened the indices of the Child-Pugh score, but only the TAA model increased the retention ratio of indocyanine green. The TAA-induced fibrosis model in Macaca fascicularis worsens fibrosis and residual liver function, mimicking Child-Pugh grade B. Given that our model was evaluated by clinical indices, it could be applicable to preclinical research.