皮肤光老化的激光治疗日益受到各方关注，但其分子机制尚不明确。因此，研究其作用的分子机制将为激光更好的用于光老化治疗提供坚实理论依据。研究表明，皮肤抗氧化能力增强、基质金属蛋白酶活性下降及前胶原蛋白合成增加是激光抗皮肤光老化的关键环节，但具体机制尚不明确。最新研究显示，S100A8蛋白下调抑制RAGE受体激活、进而抑制MAPK、NF-κB信号通路及下游转录因子AP-1，这可能是联系上述关键环节的重要途径。本研究以光老化小鼠模型、HaCaT细胞、原代成纤维细胞为实验对象，采用细胞培养、细胞转染、RT-PCR、Western blot 、Elisa等方法研究1064-nm及595-nm激光抗皮肤光老化中S100A8蛋白、RAGE受体及其介导的MAPK、NF-κB信号通路及下游AP-1所发挥的作用，阐明激光作用的具体分子机制及作用靶点，以便为激光治疗皮肤光老化机制提供初步的分子生物学理论依据。

Laser treatment of skin photoaging has attracted increasing attention, but the molecular mechanism is still not clear. Therefore, mechanism research of laser nonablative rejuvenation may provide a solid theoretical basis for its clinical use. Enhanced antioxidant capacity of skin, decreased matrix metalloproteinase activity and upregulation of procollagen synthesis are believed to be the key links of laser treatment of skin photoaging, but the exact mechanism is unknown. Recent studies have shown that the inactivation of RAGE receptor by downregulation of S100A8 activation further inhibiting the MAPK, NF-κB signaling pathways and downstream transcription factor AP-1 may be an important pathway to contact those key links. In this research, experimental subjects, including photo-aging mouse model, HaCaT cells and primary fibroblast cells, will be used to study the roles that S100A8, RAGE, MAPK, NF-κB and AP-1 play in 1064-nm and 595-nm laser treatment of skin wrinkles and to clarify the specific molecular mechanisms and crucial biological targets of laser nonablative rejuvenation by means of cell culture, cell transfection, RT-PCR, Western blot and Elisa, in order to provide a preliminary theoretical basis of molecular biology for the laser treatment of skin photoaging.