Chen Tiejun, Hou Hu, Fan Yan, Wang Shikai, Chen Qianru, Si Leilei, Li Bafang
College of Food Science and Engineering, Ocean University of China, No.5, Yu Shan Road, Qingdao, Shandong Province 266003, PR China.
College of Food Science and Engineering, Ocean University of China, No.5, Yu Shan Road, Qingdao, Shandong Province 266003, PR China.
J Photochem Photobiol B. 2016 Dec;165:34-41. doi: 10.1016/j.jphotobiol.2016.10.015. Epub 2016 Oct 14.
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 1200Da, 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.
长期暴露于紫外线（UV）照射会导致皮肤光老化。本研究旨在确定源自太平洋鳕鱼皮的明胶水解物（CH）的抗光老化机制。通过小鼠皮肤光老化模型，采用定量实时逆转录-聚合酶链反应（qRT-PCR）和酶联免疫吸附测定（ELISA）方法，研究CH对紫外线照射后基质金属蛋白酶（MMPs）及信号通路的影响。CH的平均分子量为1200Da，每1000个残基中有273个为疏水残基，Gly-Pro和Gly-Leu序列以及C末端的Arg在CH中频繁出现。CH改善了光老化皮肤中胶原纤维的病理变化，并显著抑制了胶原含量的降低。此外，CH抑制了光老化皮肤中间质胶原酶（MMP-1）、基质溶解素1（MMP-3）和明胶酶（MMP-9）的上调表达。此外，CH通过增加基质金属蛋白酶组织抑制剂（TIMPs）的含量来抑制MMPs的活性。CH显著降低了丝裂原活化蛋白激酶（MAPK）信号通路中紫外线照射依赖性上调的ERK和p38磷酸化水平。此外，它通过下调负责调节MMPs表达的两个转录因子c-Jun和c-Fos的mRNA水平来抑制活化蛋白1（AP-1）的激活。CH可通过抑制MMPs的表达和活性有效预防紫外线照射引起的皮肤光老化。
