OBJECTIVE： To study the effects of salvianolic acid B （Sal B） on angiotensin Ⅱ （Ang Ⅱ）-induced cardiac fibroblast proliferation， secretion of type Ⅲ collagen， protein expressions of matrix metalloproteinase 9 （MMP-9）， Smad2/3， Smad7， and explore its mechanism of anti-myocardial fibrosis. METHODS： Cells were divided into blank control group （culture medium） Ang Ⅱ model group， Sal B low-dose， medium-dose， high-dose groups （12.5， 25， 50 μmol/L）. After cultured 1 h by blank or drug-containing culture， except for blank control group， cells in other groups were added 1 μmol/L Ang Ⅱ to induce proliferation. for 24 h. MTT method and hematoxylin-eosin staining method were adopted investigate the effect of Sal B on proliferation. Western blot method was adopted to detect the effects of Sal B on protein expressions of type Ⅲ collagen， MMP-9， Smad2/3， Smad7. RESULTS： Compared with blank control group， cells in Ang Ⅱ model group were significantly proliferated， protein expressions of type Ⅲ collagen， MMP-9， Smad2/3 were obviously enhanced， protein expression of Smad7 was obviously weakened， with statistical significances （P＜0.05）. Compared with Ang Ⅱ model group， the cell proliferation in Sal B groups were inhibited， protein expressions of type Ⅲ collagen， MMP-9， Smad2/3 were weakened， while protein expression of Smad7 was enhanced. Except the protein expression of type Ⅲ collagen in Sal B low-dose and medium-dose groups， the protein expression of Smad2/3 in Sal B high-dose group did not change significantly， other indexes had statistical significances （P＜0.05）. CONCLUSIONS： The anti-myocardial fibrosis effect of Sal B may be associated with inhibiting the proliferation of cardiac fibroblasts， down-regulating protein expressions of type Ⅲ collagen， MMP-9， Smad2/3 and up-regulating protein expression of Smad7.