Suppressive effect of administration of recombinant human thioredoxin on cutaneous inflammation caused by UV

Abstract

Thioredoxin (TR X) is small ubiquitous protein, which regulates cellular redox status and scavenges reactive oxygen species (ROS). TR X has been shown to exert suppressive effect on skin inflammation where oxidative stress is involved in its pathogenesis. We investigated the effect of TR X on UVB response. Ear swelling after UVB irradiation was significantly reduced in TR X-transgenic mouse compared with wild-type mouse. Furthermore, we have demonstrated that intraperitoneal administration of recombinant human thioredoxin (rhTR X) also reduced acute skin inflammatory reaction, such as skin erythema and edema. Histologically, inflammatory cells including neutrophils and lymphocytes were significantly reduced and average size of the caliber of blood vessels were also reduced in rhTR X-injected mice. The number of apoptotic keratinocytes, were significantly reduced in rhTR X-injected mice. Immunohistochemical intensity of 8-hydroxy-2'-deoxyguanosine was strikingly reduced in rhTR X-injected mouse. Western blotting showed that administration of rhTR X inhibited phosphorylation of p38 mitogen-activated protein kinases and c-Jun NH2-terminal kinase, which play important roles in inflammatory and apoptotic signaling. These findings indicated that rhTR X attenuated inflammatory and apoptotic responses by UVB. Possible mechanisms for this might be via redox regulation of stress signaling and reduction of reactive oxygen species. We discussed the future use of TR X for sedative use of skin inflammation. © 2013 Landes Bioscience.