Topically Applied Taurine Chloramine Protects against UVB-Induced Oxidative Stress and Inflammation in Mouse Skin.

Seong Hoon Kim,Young-Joon Surh,Chaekyun Kim,Hye-Won Yum,Su-Jung Kim,Young-Ger Suh,Kyeojin Kim,Seung Hyeon Kim

doi:10.3390/antiox10060867

Abstract

Excessive exposure to solar light, especially its UV component, is a principal cause of photoaging, dermatitis, and photocarcinogenesis. In searching for candidate substances that can effectively protect the skin from photodamage, the present study was conducted with taurine chloramine (TauCl), formed from taurine in phagocytes recruited to inflamed tissue. Irradiation with ultraviolet B (UVB) of 180 mJ/cm2 intensity caused oxidative damage and apoptotic cell death in the murine epidermis. These events were blunted by topically applied TauCl, as evidenced by the lower level of 4-hydroxynonenal-modified protein, reduced proportions of TUNEL-positive epidermal cells, and suppression of caspase-3 cleavage. In addition, the expression of two prototypic inflammatory enzymes, cyclooxygenase-2 and inducible nitric oxide synthase, and transcription of some pro-inflammatory cytokines (Tnf, Il6, Il1b, Il10) were significantly lower in TauCl-treated mice than vehicle-treated control mice. The anti-inflammatory effect of TauCl was associated with inhibition of STAT3 activation and induction of antioxidant enzymes, such as heme oxygenase-1 and NAD(P)H:quinone oxidoreductase 1, through activation of nuclear factor erythroid 2-related factor 2.

Highlights

Aberrant overexpression of COX-2 and inducible nitric oxide synthase (iNOS) has been reported in murine models of dermatitis and photocarcinogenesis induced by ultraviolet B (UVB) irradiation [24,25]
taurine chloramine (TauCl) reduces the expression of proinflammatory factors by fortifying antioxidant systems and inhibiting oxidative cell death in mouse skin
It protects against UVBinduced skin inflammation by promoting the expression of Nrf2-mediated antioxidant/antiinflammatory enzymes, while suppressing pro-inflammatory gene expression (Figure 7)

Summary

Introduction

Excessive exposure to solar light, especially its UV component, is a principal cause of photoaging, dermatitis, and photocarcinogenesis. Irradiation with ultraviolet B (UVB) of 180 mJ/cm intensity caused oxidative damage and apoptotic cell death in the murine epidermis. These events were blunted by topically applied TauCl, as evidenced by the lower level of 4-hydroxynonenal-modified protein, reduced proportions of TUNEL-positive epidermal cells, and suppression of caspase-3 cleavage. UVB directly damages the skin, causing apoptosis, inflammation, and photoaging [7,8], and can induce photocarcinogenesis [9,10]. Human bodies are equipped with a distinct set of substances that counteract oxidative stress and inflammatory tissue damage.

Methods

Results

Discussion

Conclusion