OBJECTIVE To observe the effect of basic fibroblast growth factor (bFGF) on the outcome of myofibroblasts in burn wounds, and to further explore the mechanism of bFGF on wound healing. METHODS Seventy-two Wistar rats were anaesthetized and put into hot water at the temperature of 98 degrees C with their back hair cut so as to cause full-thickness scald injury with an area of 30% of the total body surface. Then the rats were randomly divided into two groups of 36 mice: pure thermal injury group (administered with sterilization and dressing every other day for three times) and bFGF treatment group (administered locally with bFGF every other day in addition to the routine dressing). Three hours, six hours, one day, three days, seven days, and fourteen days after scalding samples of skin wound was taken, six rats for each time-point. Six rats were put into water at the temperature of 37 degrees C as controls and their skin samples were taken 8s after. In situ hybridization and immunohistochemical techniques were employed to detect the expression of caspase mRNA and proteins. alpha-smooth muscle actin (ASMA), and transforming growth factor-beta1 (TGF-beta1) were detected by immunohistochemical staining at different time points after scalding. RESULTS No obvious difference of ASMA expression in dermal tissues was seen at the early stage of injury. The number of cells with positive ASMA expression began to increase 1 approximately 3 days after and reached the peak by the 7th day after scalding, and then decreased gradually. The ASMA expression in bFGF group was remarkably increased by the 7th day, significantly higher than that in the pure thermal injury group (P < 0.05). By the 14th day, the ASMA expression in the bFGF group was still significantly higher than that in pure thermal injury group (P < 0.01), however, it was much lower than that in the bFGF group by the 7th day. By the 14th days after scald injury. The number of TGF-beta1 positive cells began to increase since the 3rd hour after scald injury and began to decrease by the 14th day in both experimental groups. However, the TGF-beta1 expression in bFGF group was stronger than that in pure thermal injury group. The expressions of caspase-3 mRNA and protein in bFGF group changed in the same way as in the simple injured group. Three hours after injury, the expression of caspase-3 mRNA was lower in bFGF group than in pure injury group (P < 0.05). Then the expression decreased till the 3rd day. Six hours after injury, no difference in the expression of caspase-3 mRNA was found between the two experimental groups. The expression of caspase-3 reached its second peak by the 7th day and then decreased again. However, the first expression peak of the bFGF group was lower than that of the pure thermal injury group, however, the second peak of the bFGF group was higher. CONCLUSIONS Myofibroblasts may play a critical role in wound closure and healing. bFGF treatment may increase the expression of TGF-beta1 and have a potential synergistic effect with other growth factors to stimulate the apoptosis of myofibroblasts during wound healing.