Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide.

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.