| Background Recent study showed that botμLinum toxin A(BTXA)coμLd prevent scar formation by reducing skin tension around scars.Because fibroblast(FB)is the main power cell to induce wound contraction,the purpose of our research is to explore the effects of BTXA on the proteins that affect the contraction of fibroblasts.Moreover,the optimal dose of BTXA on hypertrophic scars has not yet been determined.The current study investigated the effect of different doses of BTXA on scar formation.We used some methods(TUNEL,Western blot and immunohistochemical staining)in rabbit ears to explore the molec μ Lar mechanism of BTXA by comparing the phosphate-buffered saline(PBS)and triamcinolone acetonide(TAC)treatment.Objective To explore the molec μ Lar mechanism of BTXA on preventing scar formation by comparing the phosphate-buffered saline(PBS)and triamcinolone acetonide(TAC)treatment.Methods 18 rabbits’ ears of New Zealand rabbits were used to establish hypertrophic scar model.These wounds were divided into four groups as group B(treated with deferent dosage of BTXA),group T(treated with TAC),group S(not treated)and group C(normal skin).Fibroblast apoptosis was detected by the method of TUNEL.Collagen I,ⅡI and TGF-β1 expression were examined by Western blot.The immunohistochemical staining and computerized image analysis were used to measure the optical density(OD value)of positive staining of α-SMA and myosin Ⅱ.ResμLts and Conclusions With increasing BTXA dose,the apoptotic rates increased.Western blot showed that Collagen fibrils and TGF-β1 proteins were expressed lower with the increasing of dose of BTXA.α-SMA and myosin Ⅱ in Group B were significantly decreased than those in Group T,moreover,more myosin Ⅱ can be reduced with high concentrations of BTXA(2.0 IU).It was shown that BTXA coμLd induce fibroblast apoptosis and inhibit the expression n of α-SMA and myosin Ⅱ,which can inhibit FB contraction.It plays a positive role in the treatment of scar. |
