Background: Hepatic fibrosis is a serious disease that causes around 1.5 million deaths annually due to cirrhosis and primary liver cancer. It is a pathological process that leads to the liver tissue losing its natural architecture and a severe accumulation of extracellular matrix proteins. Vitamin D3 is a sunlight hormone which promotes proliferation of cells, differentiation, apoptosis, and angiogenesis associated with hepatic parenchyma. Aim of study: Our aim was to determine the potential of vitamin D to inhibit the progression of hepatic fibrosis induced in albino rats. Material & Methods: In a recent study, Thioacetamide was used to induce hepatic fibrosis in a rat model. Randomly, forty albino rats were classified into four identical groups (ten rats per group). These groups were Healthy group, fibrotic group, Prophylactic group with vitamin D and treated group with vitamin D. Biochemical and histological analysis were evaluated. By using ELISA, IL-6, IL-1B, and TNF-α were examined. Results: The results revealed that there was very highly significant decreased (P˂0.0001) in ALT, ALP, AST, Total Bilirubin and Direct Bilirubin levels in groups which treated with vitamin D (G3, G4) compared with fibrotic group (G2), while there was highly significant increase in albumin (p˃0.001) in vitamin D treated group. Liver sections from vitamin D groups showed markedly decreased hepatic lesions. We found a very highly significant effect of vitamin D on IL-6, IL-1B, and TNF-α levels. Conclusion: There are a potential therapeutic value and antifibrotic effects of Vitamin D on hepatic fibrosis in the thioacetamide model.