Immune response plays an important role in the development of hepatic
fibrosis. In the present study, we investigated the effects of
quercetin on
hepatitis and hepatic
fibrosis induced by immunological mechanism. In the acute
hepatitis model,
quercetin (2.5 mg/kg) was injected iv into mice 30 min after
concanavalin A (Con A) challenge. Mice were sacrificed 4 or 24 h after Con A injection, and
aminotransferase tests and histopathological sections were performed. Treatment with
quercetin significantly decreased the levels of
alanine aminotransferase (ALT) and
aspartate aminotransferase (AST). Consistent with this observation, treatment with
quercetin markedly attenuated the pathologic changes in the liver. A hepatic
fibrosis model was also generated in mice by Con A challenge once a week for 6 consecutive weeks. Mice in the experimental group were treated with daily iv
injections of
quercetin (0.5 mg/kg). Histopathological analyses revealed that treatment with
quercetin markedly decreased
collagen deposition, pseudolobuli development, and hepatic stellate cells activation. We also examined the effects of
quercetin on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and
transforming growth factor beta (TGF-β) pathways by immunohistochemistry and real-time
reverse transcriptase-polymerase chain reaction (RT-PCR). NF-κB and TGF-β production was decreased
after treatment with
quercetin, indicating that the antifibrotic effect of
quercetin is associated with its ability to modulate NF-κB and TGF-β production. These results suggest that
quercetin may be an effective therapeutic strategy in the treatment of patients with liver damage and
fibrosis.