Abstract
There is growing evidence that prevention of skin photoaging by oral administration of food-derived proteins hydrolysates is intricately linked to its alleviation against oxidative stress through modulation of the signaling pathway. Previously, walnut protein hydrolysates (WPHs) were prepared by enzymatic hydrolysis by our group and exhibited excellent anti-photoaging effect through regulation of extracellular matrix metabolism and the NF-κB signaling pathway. However, its response to oxidative stress and cascade mechanism remain unknown. In the present study, Sprague-Dawley rats were exposed periodically to UV irradiation and orally administered with WPHs to further examine the effects of WPHs on the redox state, MAPK/AP-1 and TGF-β/Smad signaling pathways, type I procollagen synthesis, and histopathological impairments in photoaging skin. Intervention with WPHs for 18 weeks significantly alleviated the photoaging morphology, enhanced the antioxidant components, and downregulated the phosphorylation levels of extracellular signal-regulated kinase (ERK) and C-Jun N-terminal kinase (JNK and p38 proteins) in photoaging tissues, while significant alterations on the gene expression levels of ERK, JNK and p38 were not observed. Meanwhile, WPHs significantly activated the TGF-β/Smad signaling pathway and type I procollagen production. Furthermore, histopathological analysis illustrated that WPHs predominately attenuated epidermal hyperplasia, reduced inflammatory filtration, and promoted the deposition of collagen fibers in photoaging skin. Altogether, the underlying mechanism of WPHs attenuating skin photoaging might lie in the synergistic modulation by increasing the antioxidant capacity, modulating the MAPK/AP-1/MMP-1 and TGF-β/Smad signaling pathways, stimulating the synthesis of type I procollagen, and restoring the impaired architecture structure. Our findings suggest that WPHs are promising agents for preventing skin photoaging.
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