AimTo investigate the signaling pathways involved in the process which adipophilin induced the intracellular lipid accumulation.MethodsWe obtained the RAW2647 cells of high or low expression of adipophilin by constructing retroviral vector.Then the cells were incubated with 300 nmol/L of Calphostin C (PKC inhibitor) for 16 h or incubated with 50 mg/L ox-LDL simultaneously.The expression of ACAT1 was detected by RT-PCR and Western blot. ResultsThe results showed that RAW2647 cells with high expression of adipophilin increased the expression of ACAT1, and decreased in cells of low expression of adipophilin.Calphostin C inhibited the expression of ACAT1 in the cells with high or low expression of adipophilin.Compared with the cells incubated without Calphostin C, the difference was significant.Calphostin C also inhibited the expression of ACAT1 when incubated the cells of high expression of adipophilin with oxLDL for lipidloading.Both mRNA and protein were significantly decreased after incubated for 16 h and the difference was significant compared with the control.In the condition of lipidloaded, Calphostin C could inhibit ACAT1 expression timedependently in cells of low expression of adipophilin.ConclusionThe results indicated that PKC signaling molecules affected adipophilin expression and further affected the expression of ACAT1.It suggests that PKC signal could be related to adipophilin causing intracellular lipid accumulation.