Background: Cirrhosis is a condition come from excessive liver fibrosis and followed by serious second diseases. 1.3 million people are died of cirrhosis in a year but there is no effective therapeutic medicine. α7 nicotinic acetylcholine receptor (α7nAChR), initially found a receptor related to neurotransmission, expresses on immune cells and activation of this receptor leads anti-inflammatory effect. However, there is few reports showing the relationship between α7nAChR and fibrosis.
Aim: Using α7nAChR knocked out mice (α7 KO), we investigated whether α7nAChR has any effect on liver fibrosis.
Methods: Liver fibrosis model mice were established with carbon tetrachloride (CCl₄, 1 ml/kg, twice a week). The amount of collagen and pro-fibrotic mRNA expressions in livers were measured at 1.5 and 4 weeks.
Results: α7 KO treated with CCl₄ showed significant decrease in liver fibrosis at 4 weeks compared to wild type mice (WT). Furthermore, mRNA expressions of Acta2, TGF-β1 and Col1a1 in α7 KO were significantly lower than WT at 1.5 weeks.
Conclusion: Increase of pro-fibrotic mRNA expression and liver fibrosis induced by CCl₄ were alleviated in α7nAChR KO mice. These data suggested that α7nAChR might be a therapeutic target for cirrhosis.