Abstract

This study aimed to determine the effect of topically applied Laminaria polysaccharide (LP) on skin aging. We applied ointment containing LP (10, 25, and 50 μg/g) or vitamin E (10 μg/g) to the dorsal skin of aging mice for 12 months and young control mice for 4 weeks. Electron microscopy analysis of skin samples revealed that LP increased dermal thickness and skin collagen content. Tissue inhibitor of metalloprotease- (TIMP-) 1 expression was upregulated while that of matrix metalloproteinase- (MMP-) 1 was downregulated in skin tissue of LP-treated as compared to untreated aging mice. Additionally, phosphorylation of c-Jun N-terminal kinase (JNK) and p38 was higher in aging skin than in young skin, while LP treatment suppressed phospho-JNK expression. LP application also enhanced the expression of antioxidative enzymes in skin tissue, causing a decrease in malondialdehyde levels and increases in superoxide dismutase, catalase, and glutathione peroxidase levels relative to those in untreated aging mice. These results indicate that LP inhibits MMP-1 expression by preventing oxidative stress and JNK phosphorylation, thereby delaying skin collagen breakdown during aging.

Highlights

  • Skin is the largest organ of the human body and serves as a protective barrier from environmental stressors such as heat, infection, water loss, and ultraviolet radiation

  • We demonstrated in this study that topical application of Laminaria polysaccharide (LP) can alleviate the alterations in collagen in the skin that are induced by aging and regulate the balance between matrix metalloproteinase- (MMP-)1 and tissue inhibitor of metalloproteinase- (TIMP-)1 by inhibiting Jun N-terminal kinase (JNK) phosphorylation

  • We confirmed downregulation in TIMP-1 expression in the skin of aging mice and found that LP treatment abrogated this effect as compared to aged mice skin without treatment. These results suggest that LP maintains the balance between Matrix metalloproteases (MMPs)-1 and TIMP-1, which is important for the maintenance of extracellular matrix (ECM) homeostasis

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Summary

Introduction

Skin is the largest organ of the human body and serves as a protective barrier from environmental stressors such as heat, infection, water loss, and ultraviolet radiation. In contrast to photoaging, which results from the effects of ultraviolet rays [1], intrinsic aging occurs naturally over time [2]. In addition to environmental factors, genetics, cellular metabolism, hormones, and metabolic processes contribute to natural aging. The development of age-related skin pathologies is associated with alterations in the levels of collagen in skin extracellular matrix (ECM) [3]. Matrix metalloproteases (MMPs) are the major enzymes involved in ECM degradation. MMP-1 is the predominant collagenase in the skin [4] whose activity is suppressed by tissue inhibitor of metalloproteinase- (TIMP-) 1. Given that the breakdown of collagen is a major cause of wrinkle formation, an obvious manifestation of aging [5, 6], blocking this process by inhibiting MMP activity is a potential strategy for preventing skin aging

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