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Scarring,tightly associated with fibrosis,is a significant symptomatic clinical problem Interleukin 10(IL-10)has been identified as a candidate scar-improving therapy based on preclinical studies However,the molecular mechanism of IL-10 in scar improvement is still uncertain In this study,human dermal fibroblasts stimulated with TGF-bl were treated with IL-10 to analyze the mRNA and some of proteins’expression levels of type Icollagen(Coll),type Ⅲ collagen(C013),alpha-smooth muscle actin(a-SMA),matrixmetalloprotemase-1(MMPI),M2VIP2,M2VIP8.and tissue inhibitor of metalloprotemase 1(TIMPl),TIMP2.byreal-time PCR and Western blot,to observe a-SMA-positive fibroblasts by immunocytochemistry Thecontracture and improvement of fibroblast-populated collagen lattice(FPCL)and a murine model of woundhealing were used to evaluate the scar-improving effects by histological staining The results showed that IL-10 can significantly down-regulate the mRNA and protein expression levels of Coll,C013,a-SMA,andup-regulate the mRNA expression levels of MMPI and MMP8,and decrease a-SMA-positive fibroblasts FPCLanalysis showed that the IL-10(20ng/m1)can significantly inhibit the contracture,improve the architecture of FPCL Wounds iNected with IL-10 demonstrated that the appearance of scar was improved,the wound marginof scarring was narrow-,and the deposition of collagens(Coll and C013)in regenerated tissue was relieved These results provide direct evidences that IL-10 has the inhibitor?"effects on the excessive deposition of extracellular matrix components and fibroblast-to-myofibroblast transition,and show-that IL-10 has thepotential therapy in prevention and reduction of skin scarring.