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.