【摘要】 目的探讨IL1(IL1α,IL1β)对长波紫外线(UVA)辐射后成纤维细胞基质金属蛋白酶(matrixmetalloproteinases,MMPs)表达的影响机制。方法用ELISA法检测UVA辐射后成纤维细胞培养上清MMP1和MMP2的表达。接着用IL1α和IL1β分别处理UVA辐射后的成纤维细胞,用Western免疫印迹法检测其丝裂原活化蛋白激酶(MAPK)的活性;用RTPCR方法检测cfos和cjun的mRNA表达。结果不同剂量UVA(0,1,5,10J/cm2)辐射的成纤维细胞分泌MMP1逐渐上升,对MMP2分泌没有影响。IL1α和IL1β(0,1,10,100ng/ml)促进UVA(10J/cm2)辐射成纤维细胞的MAPK活性表达,并以剂量依赖方式促进cjun的mRNA表达。IL1α还显著增加cfosmRNA表达,但IL1β对cfosmRNA表达无明显影响。IL1α和IL1β促进UVA辐射成纤维细胞分泌MMP1,于100ng/ml时有显著性差异(P均<0.05),但对MMP2分泌无明显影响。结论UVA辐射成纤维细胞分泌MMP1增加,对MMP2分泌没有影响。IL1(IL1α和IL1β)通过促进MAPK活性和cjunmRNA表达,IL1α还促进cfosmRNA表达使UVA辐射成纤维细胞MMP1表达增加,表明IL1在皮肤光老化的真皮胶原过度降解中发挥着重要的作用。更多还原

【Abstract】 Objective To explore the mechanism of IL-1(IL-1α,IL-1β)on matrix metalloproteinase(MMP) production of UVA-irradiated fibroblasts.Methods MMP-1 and MMP-2 production in UVA-irradiated fibroblasts culture medium was detected by ELISA. UVA-irradiated fibroblasts were treated with IL-1α or IL-1β separately,which mitogen-activated protein kinase(MAPK) expression was determined by Western immunoblot,c-fos and c-jun mRNA were detected by RT-PCR,MMP-1 and MMP-2 production was detected by ELISA.Results Different dosage of UVA(0,1,5,10 were J/cm2) increased gradually MMP-1 production of fibroblasts but had no effects on MMP-2 production.IL-1α and IL-1β(0,1,10,100 ng/ml)dose-dependently promoted MAPK activity and c-jun mRNA expression of UVA(10 J/cm2)-irradiated fibroblasts.IL-1α significant increased c-fos mRNA expression too,while IL-1β had no significantly effects on c-fos mRNA expression.IL-1α and IL-1β promoted MMP-1 production of UVA (10 J/cm2)-irradiated fibroblasts while had no significant effects on MMP-2 production,significant difference was observed at dose 100 ng/ml (P<0.05). Conclusion UVA irradiation increases MMP-1 production of fibroblasts but has no effects on MMP-2 production.IL-1(IL-1α,IL-1β)increases MMP-1 production of UVA-irradiated fibroblasts through promoting MAPK activity and c-jun mRNA expression,IL-1α increases c-fos mRNA expression also.Our data indicate that IL-1 exerts important effects on dermal collagen excessive degradation of skin photoaging.更多还原