Antioxidative Effect of Quetiapine on Acute Ultraviolet-B-Induced Skin and HaCaT Cell Damage

Pengcheng Xu,Wei Wu,Yuan Yan,Min Zhang,Lin Zhang,Yinghua Chen,Lu Zhang,Xueer Wang

doi:10.3390/ijms19040953

Pengcheng Xu, Wei Wu + Show 6 more

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https://doi.org/10.3390/ijms19040953

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Abstract

Quetiapine is a new type of antipsychotic drug, with effective protection of pheochromocytoma PC12 cells from oxidative stress-induced apoptosis. Ultraviolet-B radiation can increase reactive oxygen species (ROS) production, resulting in significant inflammatory responses in damaged skin. Thus, the purpose of this study is to explore whether quetiapine protects the skin from intermediate-wave ultraviolet (UVB)-induced damage through antioxidant stress. In vivo, we found quetiapine treatment was able to significantly decrease skin thickness, erythema, and edema, as well as inflammation compared to control group. Moreover, quetiapine treatment increased the activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In addition, it reduced the production of malondialdehyde (MDA), a kind of oxidized lipid. In vitro, we found that quetiapine blocked UVB-induced intracellular ROS generation and maintained the cell activity at a normal level. Furthermore, we tested the phosphorylation of p38 both in vivo and in vitro, and we found that quetiapine could inhibit phosphorylation of p38, which is caused by UVB irradiation. We concluded that quetiapine was able to relieve UVB-induced skin damage through its antioxidative properties. These effects might be associated with p38 MAPK signaling pathway.

Highlights

Environmental pollution has contributed to the destruction of the atmospheric ozone layer, which has increased ultraviolet (UV) radiation levels
UVB radiation often causes an acute inflammatory response; in order to further verify the protective effect of quetiapine, we examined the degree of inflammatory infiltration in different groups
Tissue damage caused by acute UVB is due to the apoptosis, inflammation and oxidative damage of keratinocytes, leading to epidermis damage and the loss of barrier function [11,12]

Summary

Introduction

Environmental pollution has contributed to the destruction of the atmospheric ozone layer, which has increased ultraviolet (UV) radiation levels. UV radiation accounts for roughly 13% of sunlight, and it is divided into longwave UV (UVA), intermediate-wave UV (UVB), and shortwave UV (UVC). UVC is completely absorbed by the atmosphere, and only some UVB and UVA radiation reaches the surface of the earth [4]; thereof, UVB damage is often associated with oxidative stress and inflammation. Reactive oxygen species (ROS) refers to a series of active oxidation products directly or indirectly, including superoxide, etc. Vitiligo and others that affect beauty are closely related to oxidative stress [5]. UVB (between 290 and 320 nm) exerts the greatest effect on people and has been significantly researched in recent years

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