摘要：Vitamin B12 contains a cobalt complex and accumulates at high levels in the liver. Vitamin B12 was examined for its hepatoprotective effect on dimethylnitrosamine-induced liver injury in mice. Vitamin B12 decreased the blood levels of aspartate aminotransferase and alanine aminotransferase, and clearly inhibited the overaccumulation of collagen fibrils. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of the liver showed that the gene expression of α-smooth muscle actin and heat-shock protein 47, which are markers of fibrosis, were suppressed by vitamin B12 administration. Our findings indicate that vitamin B12 could be an effective hepatoprotective agent.
