Objective·To investigate the effects of a novel chitosan-silver nitrate gel (CSNG) dressing on anti-septic in wound healing.Methods·By using the ion membrane,the release rate of the new composite materials of silver ion was tested in vitro.Meanwhile,the anti-septic effects of CSNG on methicillin resistant Staphylococcus aureus (MRSA),Escherichia coli and Candida albicans were tested by colony counting.The rat wound healing model was used to detect the ability of new material to kill MRSA in vivo.Results·Compared with control group,the release of silver ions of CSNG was much slower.Sterilization experiment showed that CSNG killed the MRSA,Escherichia coli and Candida albicans much more efficiently,compared to that in the other treatments.Animal experiments also showed that CSNG promoted the rats of wound healing.Conclusion·Combining chitosan with silver nitrate and supplementary material could develop a novel chitosan-silver nitrate gel material,which not only has the obvious effects on antibacterial,but also on promoting wound healing.

Objective·To investigate effect and the possible molecular mechanism of JQ1,a specific inhibitor of bromodomain containing protein 4,on human hypertropic scar.Methods·Primary fibroblasts were isolated from human hypertrophic scars and treated with JQ-1 of different concentrations (0.1,0.5,1.0,2.0,2.5,and 12.5μmol/L) for 48 h.Then CCK-8 kit and wound healing assay were used to measure proliferation and migration of the fibroblasts.ELISA was adopted to detect the levels of collagen type Ⅰ (COL Ⅰ) and TGF-β1 after JQ-1 treatment for 24 h.Thirty-six nude mice were used for hypertrophic scar models.Human hypertrophic scars (1.0 cm× 1.0 cm×0.5 cm) were grafted subcutaneously at the backs of nude mice to establish scar animal models.After 4 weeks,the nude mice were averagely divided into two groups,i.e.JQ-1 group and DMSO group,which were respectively injected with 0.5 μmol/L JQ-1 and 0.1％ DMSO each mouse every day.COL Ⅰ / Ⅲ and α-smooth muscle actin (α-SMA) were examined by immunohistochemical method and sirius red staining.Results·Cell experiments showed that JQ-1 with the concentration of 0.5 μmol/L and above significantly inhibited proliferation of fibroblasts (P＜0.01).JQ-1 inhibited migration of fibroblast (P＜0.01).JQ-1 inhibited secretion of COL Ⅰ and TGF-β1 of fibroblasts (P＜0.01).Animal experiments showed that concentration and proportion of COL Ⅰ / Ⅲ in JQ-1 group decreased compared to DMSO group (P＜0.05).α-SMA protein expression in JQ-1 group also decreased (P＜0.05).Conclusion·JQ-1 can inhibit proliferation,migration,secretion of COL Ⅰ,and production of TGF-β1 of human sear fibroblasts in vitro;it can also inhibit secretion of COL Ⅰ /Ⅲ and fibroblast-myofibroblast differentiation in the human hypertrophic scars in nude mice.

In recent years, researchers have found that CD26 (dipeptidyl peptidase 4) is closely related to the formation and development of many fibrotic diseases. Hypertrophic scar, keloid, and other skin fibrosis diseases are major problems nowadays, which may affect the patient′s appearance and cause joints deformity and dysfunction due to scar contracture. This article briefly reviews the relationship between CD26 and hypertrophic scar and keloid to provide new insights into the treatment of skin fibrotic diseases.