ABSTRACT
BACKGROUND: Transforming growth factor-β(TGF-β) is an essential factor for pathological scar formation. Smad protein group is the signal protein of lower reaches of TGF-β receptor. Asiaticoside can inhibit proliferation of fibroblasts and synthesis of collagen to reduce TGF-β expression in the scar.OBJECTIVE: To study the mechanism of asiaticoside on proliferation of scar fibroblasts and phosphorylated Smad2 and Smad7.DESIGN: Controlled study with observation, in which cell was taken as the object.SETTING: Department of burn and plastic surgery of a hospital affiliated to a university.PARTICIPANTS: The experiment was performed in Surgical Laboratory in Sun Yat-sen University from April 2002 to March 2003. The specimens were selected from 6 inpatients receiving plastic operation due to hyperplasic scar including 3 male and 3 female cases aged varied from 1 to 35 years. The hyperplasic scar fibroblasts were obtained generated from original culture in laboratory of surgical department.INTERVENTIONS: In the research, the experiment group and the control group were divided. In the experiment group, asiaticoside was applied on fibroblasts; in the control group, asiaticoside was not prescribed. The changes of every index were observed before and after medication.MAIN OUTCOME MEASURES: ① Effect of asiaticoside on expression of phosphorylated Smad2 and Smad7; ② Effect of asiaticoside on cell cycle and apoptosis.RESULTS: Asiaticoside inhibited scar fibroblasts entering M phrase from S phrase and reduced the content of phosphorylated Smad2 in fibroblasts, which did not present significant difference in two groups ( t = 1.53, P =0.08).The content of Smad7 in the cells was (50. 80 ± 22.40)% in the experiment group and (32.18 ± 17.84)% in the control group, which indicated significant difference ( t = 2. 17, P = 0. 024).CONCLUSION: Asiaticoside inhibits scar formation by Smad passage.
ABSTRACT
@#ObjectiveTo explore the role of vascular endothelial growth factor(VEGF) in the growth and development of hypertrophic scar.MethodsThe burn wound samples of various stages were selected from transition of wound granulation tissue to scar and in long-persisting post-burn hypertrophic scar, and the concentrations of VEGF protein were detected using enzyme-linked immunosorbent essay (ELISA) method. ResultsThe tissue homogenate concentration of VEGF protein increases gradually from the wound granulation tissue to hypertrophic scar before it achieves summit concentration during 4 to 6 month. The concentration of VEGF degreases gradually after the maturation of hypertrophic scar. The high concentration of VEGF is synonymous with the large amount of capillary of the immature scar.ConclusionsThe abnormal expression of VEGF is related to the growth and development of hypertrophic scar and induces excessive and uncontrollable angiogenesis.
ABSTRACT
【Objective】 To investigate the possible mechanism of the asiaticoside used for the treatment of hypertrophic scar. 【Method】 Using microscope, electron microscope, MTT test, 3 H-TdR and 3 H-Pro line incorpo ration to study the effect of the asiaticoside on DNA synthesis and collagen bi osynthesis of fibroblast in vitro culture. 【Results】 The asiaticoside not only affected the ultrostructure of fibroblast, but also inhibted the DNA synthesis a nd collagen biosynthesis.【Conclusion】 Asiaticoside can play an important role in the prevntion and treatment of scars, the mechanism may be that the asiaticos ide can inhibted the DNA synthesis and collagen biosynthesis of fibroblast.
ABSTRACT
Objective To investigate the effects of transforming growth factor-?1 (TGF-? 1) on the synthesis of FN and ? 5? 1 integrin b y cultured human fibroblast isolated from hypertrophic scars. Methods The influence of TGF-? 1 at concentration of 0, 5, 10, 25, 50 and 100 ?g/L on the synthesis of FN in dosage was observed using ELISA, an d influence of TGF-? 1 on the synthesis of ? 5? 1 integrin was assessed b y immunohistocytochemistry and image analysis. Results TG F-? 1 could stimulate the human fibroblasts isolated from hypertrophic scars to synthesize FN and? 5? 1 integrin with dose-dependent increase at concent ration of 10～50 ?g/L and the effects TGF-? 1 on the synthesis was the stron g est at concentration of 100 ?g/L. Conclusions TGF-? 1 may exert its function on the formation of hypertrophic scars by stimulating th e synthesis of FN and ? 5? 1 integrin.