| Objectives1. To observe the effects of intense pulsed light on the cell prolifer-ation of human fibroblasts.2. To investigate the role of ERK signaling pathway and TGF-β1 in effects of intense pulsed light on the proliferation of fibroblasts.Methods1. Fibroblasts isolated from human foreskin were cultured in vitro and identified by immunocytocchemical staining.2. Fibroblasts were treated with different dose of IPL irradiation, the cell morphologcal changes were observed by light microscopy; the cell proliferation activity was detected by MTT assay, p-ERK1/2 expressions were assessed by western blot.3. In the study of intervention, the cell proliferation activity and p-ERK1/2 expressions were determined after fibroblasts treated by PD98059 (specific inhibitor of ERK) and IPL irradiation+PD98059.4. Fibroblasts were treated with different dose of IPL irradiation, and TGF-β1 in the supernaant liquid were measured by ELISA. Results1. Cultured cells had the normal form of fibroblasts and were stained positive for type I and III collagens and negative for keratin.2. Compared with sham-irradiation, IPL irradiation showed no notic-eable effect on the cell morphology of fibroblasts. The cell growth or cellular activity was no obviously changed by the IPL irradiation at a dose of10,18,27,36 J/cm2(P>0.05); When the dose of IPL was 36 J/cm2×2, the cell proliferation activity was markedly increased 24 and 48 hours after the IPL irradiation(P<0.05). The p-ERK1/2 expressions was no obviously changed by the IPL irradiation at a dose of 36 J/cm2, when the dose of IPL was 36 J/cm2x2, the p-ERK1/2 expressions was decreased.3. The cell proliferation and p-ERK1/2 expressions were obviously inhibited by PD98059 (P<0.05).4. Compared with sham-irradiation, the TGF-β1 secretion was no obviously changed by the IPL irradiation at a dose of 36 J/cm2(P>0.05), when the dose of IPL was 36 J/cm2x2, the TGF-β1 secretion was signifi-cantly enhanced (P<0.05).ConclusionIPL irradiation can induce the cell proliferation of fibroblasts, the mechanism of which mybe due to the increasing of TGF-β1 secretion but not to the ERK signaling pathway. |