Therapeutic Effect of Seawater Pearl Powder on UV-Induced Photoaging in Mouse Skin.

Siyin Han,Yuanyang Ou,Jiying Wei,Peng Liu,Weiyuan Zhang,Taijin Lan,Qiangqiang Yan,Delun Huang,Jiang Lin,Yongpei Wu,Zhenxing Chen,Yingbiao Wang,Jian-You Guo

doi:10.1155/2021/9516427

Abstract

The objective of this study was to investigate the therapeutic effect of seawater pearl powder (SPP) on ultraviolet (UV) irradiation-induced photoaging in mouse skin. The protein and trace elements in SPP were detected by liquid chromatography-mass spectrometry, atomic fluorescence spectrometry, and inductively coupled plasma-atomic emission spectrometry. The effect of SPP on treating skin damage resulting from UV-induced photoaging was observed by gross physical appearance and histopathological analysis. Oxidative stress and melanin synthesis were analyzed using biochemical method. Western blotting was applied to analyze the phosphorylation and expression levels of matrix metalloproteinase-1 (MMP-1), collagen I, and proteins involved in the mitogen-activated protein kinase (MAPK) signaling pathways (p38, ERK, and JNK). The results show that SPP has a significant therapeutic effect on UV-induced photoaging of skin and improves and restores appearance and tissue structure of mouse skin. The major mechanism may be related to reduction of expression level of MMP-1 and enhancement of collagen I production via inhibition of MAPK signaling pathway after scavenging of excess reactive oxygen species (ROS) in the UV-induced photoaged skin of mice. Meanwhile, it may also be involved in reducing melanin content by inhibiting tyrosinase activity after scavenging excess ROS in the UV-induced photoaged skin of mice. Therefore, SPP could be a good substance to treat photoaging skin. Taking cost-effectiveness and efficacy into consideration, the optimal concentration of SPP for treating photoaging skin could be 100 mg/g.

Highlights

Skin photoaging is mainly caused by environmental factors, such as ultraviolet (UV) irradiation, smoking, and chemicals
Previous studies have shown that UV irradiation-induced reactive oxygen species (ROS) mediate the phosphorylation of protein kinases through the mitogenactivated protein kinase (MAPK) signaling pathway, which involves the upregulation of extracellular signal-regulated kinases (ERK), c-Jun amino terminal kinase (JNK), and p38 [3]. e activation of the MAPK signaling pathway directly results in phosphorylation of the activator protein-1 (AP-1) complex, which upregulates the expression of matrix metalloproteinases (MMPs) [4]
UV irradiation upregulates the expression of matrix metalloproteinase-1 (MMP-1) that initiates the degradation of type I and type III collagen [5], and the degraded collagen fragments produced by MMPs downregulate new collagen synthesis in vitro and in vivo [6]

Summary

Introduction

Skin photoaging is mainly caused by environmental factors, such as ultraviolet (UV) irradiation, smoking, and chemicals. UV irradiation, such as UVA and UVB, is the primary cause of accelerated photoaging, which disrupts the balance between collagen production and degradation resulting in functional collagen loss. E activation of the MAPK signaling pathway directly results in phosphorylation of the activator protein-1 (AP-1) complex, which upregulates the expression of matrix metalloproteinases (MMPs) [4]. UV irradiation upregulates the expression of matrix metalloproteinase-1 (MMP-1) that initiates the degradation of type I and type III collagen [5], and the degraded collagen fragments produced by MMPs downregulate new collagen synthesis in vitro and in vivo [6]. Melanin overproduction can be stimulated by UV irradiation [7]. e irregular pigmentation of photoaged

Methods

Results

Discussion

Conclusion