Nicotine stimulates fibrogeneis that is mediated through α7nAChR. Our Aim was to determine the effects of nicotine on cholangiocyte (BEC) growth and profibrogenic gene expression. Methods α7nAChR expression was assessed in liver sections from normal and BDL rats and NRIC (cell line). Normal and BDL rats were treated with nicotine (24 mg/kg/BW per day) or vehicle for 2 wks by osmotic minipumps. In vivo, proliferation was determined by intrahepatic bile duct mass (IBDM) in liver sections. Collagen deposition was evaluated by Masson's trichrome staining. The effect of nicotine (1 μM, 24–48 hrs) on NRIC growth was determined by MTS assay with/without α‐bungarotoxin (ABT, α7nAChR inhibitor). Nicotine‐induced CTGF, TGFβ1, and Col1A1 gene expression was evaluated by qPCR. Results BEC expressed α7nAChR. Nicotine induced an increase in IBDM in normal and BDL rats, and increased collagen deposition surrounding bile ducts in normal and BDL rats. Nicotine‐stimulated proliferation was blocked by ABT. Nicotine stimulated CTGF, TGFβ1, and Col1A1 gene expression. Conclusion Nicotine stimulates the growth of BEC and induces profibrogenic gene expression.