Objective To investigate the effect of propofol on the gap junction function of BRL-3A cells and cisplatin-induced toxicity to rat hepatic BRL-3A cells. Methods Rat hepatic BRL-3A cell line was provided by professor Tao laboratory of department of pharmacology of our university and cultured in DMEM liquid culture medium at 37℃. The cells were randomly divided into 6 groups: group Ⅰ control (group C) ; group Ⅱ was exposed to intralipid (the solvent) 10 μg/ml (group Ⅰ) ; group Ⅲ was exposed to oleamide (gap junction function inhibitor) 25 μmol/L (group O) and group Ⅳ ,Ⅴ , Ⅵ were exposed to propofol l.5, 2.8 and 4.1 μg/ml respectively (groups P1, 2,3) . Using parachute dye-coupling assay, the dye spread rate and inhibition rate were calculated to measure the gap junction function of BRL-3 A cells. BRL-3 A cells were seeded in two different densities:high density group (seeding density = 1×105 /ml) and low density group (seeding density = 500/ml). Both groups were further divided into 5 subgroups: subgroup Ⅰ control; subgroup Ⅱ was exposed to cisplatin 2.5 μmol/L and subgroup Ⅲ ,Ⅳ ,Ⅴ were exposed to cisplatin 2.5 μmol/L + intralipid 10 μg/ml or oleamide 25 μmol/L or propofol 2.8 μg/ml respectively. The effect of propofol on the cytotoxicity of cisplatin was evaluated by standard colony-forming assay. Results The dye spread rate was significantly lower and inhibition rate higher in groups O,P1 , P2 and P3 than in group C. Propofol decreased the dye spread rate and increased inhibition rate in a concentration-dependent manner. Propofol and oleamide significantly increased colony formation rate in high density group,but had no significant effect on colony formation rate in low density group. Conclusion Propofol can inhibit the gap junction function of BRL-3A cells in a concentration-dependent manner and reduce cisplatin-induced cytotoxicity by inhibiting gap junction function.