MAPKs信号通路中的JNK及p38在UV所致皮肤光损伤机制中发挥重要作用。以往关于白黎芦醇防护皮肤光损伤机制方面的研究着眼于NF-κB、p53乙酰化、TGF-β2、ROS等角度。最近问世一种新型白藜芦醇因分子结构特殊而具有不同于传统白藜芦醇的药理特点。本课题组前期研究发现这种新型白藜芦醇可防治UV诱导的皮肤晒红、黑素沉积、免疫抑制等光损伤表现。其具体作用机制需进一步明确。本研究拟采用UVA、新型白黎芦醇、MAPKs抑制剂作用于正常及沉默SIRT1基因的人皮肤成纤维细胞，阐明新型白黎芦醇防治UVA诱导的皮肤光损伤的分子机制是否通过SIRT1 抑制MAPKs通路实现的。另外，以UVA、新型白藜芦醇、MAPKs抑制剂处理野生型及SIRT1抑制剂干预的C57BL/6小鼠，动物水平证实上述机制并据此找到防治小鼠皮肤光损伤的最佳方案。本研究将为新型白藜芦醇防治光损伤提供理论依据及新的防治策略。

JNK and p38 MAPKs via upregulation MMPs play important roles in UV-induced photodamage. Previous studies focused on NF-κB, p53 acetylation, TGF-β2 and ROS to elaborate the mechanism of resveratrol's photoprovention effects. Recently, a novel resveratrol was developed and found to have advantages over traditonal one owing to its' special molecular structure. Our preliminarily studies have showed the protective effects of the novel resveratrol on UV-induced photodamages including sunburning, pigmenataion, immunosuppression, et al. The mechanism needs to be further determined. The present study will expose normal and SIRT1-silenced human skin fibroblast to UVA, the novel resveratrol, and MAPKs inhibitors, to elaborate whether the mechanism of resveratol on UVA-induced photodamage is through SIRT1 inhibiton of MAPKs pathways. Furthermore, wildtype and SIRT1 inhibitor-dealed C57BL/6 mice will be treated with UVA, the novel resveratrol, and MAPKs inhibitors, to verify above mechinism and to found optimal modality for UV-induced photodamage on mice skin. The study will provide theory evidence for the application and a new strategy of resveratrol on photodamage.