The main objectives of this study were as follows: (1) to elucidate the role of the antifibrosis effect of CA in protecting against BDL; (2) to test whether the activity of CA against liver fibrosis is associated with the signaling mechanisms of HMGB1/TLR4/NF-κB pathway in BDL; and (3) to investigate whether CA inhibits HMGB1/TLR4/NF-κB by promoting the expression of miR-29b-3p. This evidence concerns the gene NFKB1 and Hepatic fibrosis.