Previous studies have demonstrated the important role of taurine in inhibiting proliferation of myofibroblasts(myoFb) and myocardial fibrosis.However,the underlying mechanisms are unclear.The present study was designed to shed light on this issue through exploring the signal pathways via in vitro experiments.Angiotension Ⅱ (AngⅡ) treatment significantly increased myoFb proliferation and the levels of collagens Ⅰ and Ⅲ(P＜0.05),whereas taurine,PKCαt(PKC:protein kinase C) specific inhibitor L-threo-dihydro-sphingosine(D4681),ERK1/2 inhibitor (PD98095) abrogated myoFb proliferation and collagen levels(P＜0.05,P＜0.01,respectively),and increased the G0/G1 phase rate and decreased S phase rate.Immunocytochemistry,confocal fluorescence staining and image analysis showed that taurine could inhibit the translocation and expression of p-PKCαtin membrane,and then inhibit nuclear translocation and expression of p-ERK1/2.These results have statistically significant differences compared with those of AngⅡ group(P＜0.0l).Western blot results also show that taurine could inhibit the protein expression of p-PKCαt and p-ERK1/2.We used p-PKCα specific inhibitor D4681 in order to elucidate the relationship between p-PKCα and p-ERK1/2 in signal transduction pathways.Finally,the results show that the protein expression of p-ERK1/2 and nuclear translocation were suppressed in D4681 group.