Protective effect of gelatin peptides from pacific cod skin against photoaging by inhibiting the expression of MMPs via MAPK signaling pathway

- CH alleviated photodamages to collagen fibers and reduction of collagen level.
- The activities and expressions of MMPs were inhibited when treated by CH.
- CH could enhance the level of tissue inhibitors of metalloproteinases (TIMPs).
- CH suppressed the activation of AP-1 and blocked MAPK pathway.

Chronic exposure to ultraviolet (UV) irradiation causes skin photoaging. This study was undertaken to identify the anti-photoaging mechanisms of gelatin hydrolysate (CH) derived from pacific cod skin. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and ELISA assays were used to investigate the effects of CH on matrix metalloproteinases (MMPs) and the signaling pathways after UV irradiation by using a mice skin photoaging model. The average molecular weight of CH was 1200 Da, and 273/1000 residues were hydrophobic, Gly-Pro and Gly-Leu sequences and Arg at C-terminus appeared frequently in CH. CH improved pathological changes of collagen fibers and significantly inhibited collagen content reduction in photoaging skin. Moreover, CH blocked the up-regulated expression of interstitial collagenase (MMP-1), stromelysin 1 (MMP-3), and gelatinase (MMP-9) in photoaging skin. Besides, CH suppressed the activities of MMPs by increasing the contents of tissue inhibitors of matrix metalloproteinases (TIMPs). CH significantly reduced the UV irradiation-dependent up-regulated phosphorylation of ERK and p38 in the mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, it inhibited the activation of activator protein 1 (AP-1) by down-regulating the mRNA level of c-Jun and c-Fos, which are the two transcription factors responsible for the regulation of MMPs expression. CH can effectively protect against UV irradiation-induced skin photoaging by inhibiting the expression and the activity of MMPs.

Graphical Abstract