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Updated: Jan 22, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
The Use of Antifibrotic Recombinant nAG Protein in a Rat Liver Fibrosis Model
Maha M Arafah1, Mohammad M Al-Qattan2,3,4,5, Durria A Abdulmaged-Ahmed3
1Department of Pathology, King Saud University, Riyadh, Saudi Arabia.
Objectives:
The "nAG" protein is the key protein mediating the regeneration of amputated limbs in salamanders. The senior author (MMA) developed the original hypothesis that since "nAG" is a "regenerative" protein, it must be also an "antifibrotic' protein. The antifibrotic properties were later confirmed in a rabbit skin hypertrophic scar model as well as in a rat spinal cord injury model. The aim of this study is to evaluate the potential therapeutic properties of the nAG protein in a rat liver fibrosis model.
Methodology:
Liver fibrosis was induced using intraperitoneal injections of carbon tetrachloride (CCL4). A total of 45 rats were divided equally into 3 groups: Group I (the control group) received normal saline injections for 8 weeks, Group II received CCL4 for 8 weeks, and Group III received CCL4 and nAG for 8 weeks. At the end of the experiment, the serum levels of 6 proteins (hyaluronic acid, PDGF-AB, TIMP-1, laminin, procollagen III N-terminal peptide, and collagen IV-alpha 1 chain) were measured. Liver biopsies were also taken and the stages of live fibrosis were assessed histologically.
Results:
The CCL4 treatment resulted in a significant increase in the serum levels of all 6 measured proteins. The nAG treatment significantly reduced these high levels. The degree of liver fibrosis was also significantly reduced in the CCL4/nAG group compared to the CCL4 group.
Conclusions:
nAG treatment was able to significantly reduce the serum levels of several protein markers of liver fibrosis and also significantly reduced the histological degree of liver fibrosis.
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