胶原蛋白肽修复光老化皮肤作用研究进展

Recent progress in repairing photoaged skin with collagen peptide

从体内动物试验、体内临床试验和体外细胞试验等3个方面介绍胶原蛋白肽(collagen peptide, CP)对光老化皮肤的修复作用。从体内动物试验分析CP对紫外线(ultraviolet, UV)照射下小鼠背部皮肤细胞外基质成分和抗氧化指标的影响,归纳CP通过抑制UV照射下小鼠皮肤胶原蛋白和透明质酸含量的降低从而修复光老化皮肤的作用,探讨CP通过抑制UV照射下小鼠皮肤抗氧化指标的异常变化和基质金属蛋白酶表达的升高从而分别促进胶原蛋白合成和抑制胶原蛋白降解,阐明CP修复光老化小鼠皮肤的作用机制;从体内临床试验分析口服CP对女性皮肤水合作用和胶原蛋白含量的影响,归纳CP通过抑制UV照射下女性皮肤水合作用的减弱和胶原蛋白含量的降低从而达到修复光老化皮肤的作用;从体外细胞试验及信号通路层次,分析皮肤光老化与丝裂原活化蛋白激酶(mitogen-activated protein kinases, MAPK)信号通路的激活和转化生长因子β(transforming growth factor-β, TGF-β)信号通路的抑制关系,以及CP剂量依赖性促进UV照射下皮肤成纤维细胞的增殖、迁移和黏附,增加细胞活力和伤口愈合速度,探讨CP通过抑制UV照射下皮肤成纤维细胞MAPK信号通路的激活和TGF-β信号通路的减弱从而修复光老化的皮肤成纤维细胞的作用机制。

The repair effects of collagen peptide(CP) on photoaged skin were introduced from three aspects: in vivo animal trials, in vivo clinical trials and in vitro cell trials. The effects of CP on extracellular matrix components and antioxidant indexes of mice dorsal skin under ultraviolet(UV) irradiation were analyzed from in vivo animal trials and the effects of CP on repairing photoaged skin by inhibiting the decrease of collagen and hyaluronic acid contents in mouse skin under UV irradiation were summarized. It was discussed that CP could promote collagen synthesis and inhibit collagen degradation respectively by inhibiting the abnormal changes of antioxidant indexes, the mechanism of CP repairing photoaged mouse skin was elucidated. The effects of oral CP on female skin hydration and collagen content were analyzed from in vivo clinical trials, and it was concluded that the effects of CP on repairing photoaged skin were through inhibiting the decrease of hydration and collagen content in the skin of female under UV irradiation. It was concluded that skin photoaging was closely related to the activation of mitogen-activated protein kinases(MAPK) signaling pathway and the inhibition of transforming growth factor-β(TGF-β) signaling pathway from in vitro cell trials and signaling pathway levels, and that CP could also dose-dependently promote the proliferation, migration and adhesion of skin fibroblasts under UV irradiation, thus increasing cell viability and accelerating wound healing. It was also discussed that the mechanism of CP repairing photoaged skin fibroblastswas through inhibiting the activation of MAPK signaling pathway and the weakening of TGF-β signaling pathway in skin fibroblasts under UV irradiation.