Abstract

Ultraviolet-B radiation (285–320 nm) elicits a number of cellular signaling elements. We investigated the preventive effect of linalool, a natural monoterpene, against UVB-induced oxidative imbalance, activation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling in HDFa cells. We observed that linalool treatment (30 μM) prevented acute UVB-irradiation (20 mJ/cm2) mediated loss of activities of antioxidant enzymes in HDFa cells. The comet assay results illustrate that linalool significantly prevents UVB-mediated 8-deoxy guanosine formation (oxidative DNA damage) rather than UVB-induced cyclobutane pyrimidine (CPD) formation. This might be due to its ability to prevent UVB-induced ROS formation and to restore the oxidative imbalance of cells. This has been reflected in UVB-induced overexpression of MAPK and NF-κB signaling. We observed that linalool inhibited UVB-induced phosphorylation of ERK1, JNK and p38 proteins of MAPK family. Linalool inhibited UVB-induced activation of NF-κB/p65 by activating IκBa. We further observed that UVB-induced expression of TNF-α, IL6, IL-10, MMP-2 and MMP-9 was modulated by linalool treatment in HDFa cells. Thus, linalool protects the human skin cells from the oxidative damages of UVB radiation and modulates MAPK and NF-κB signaling in HDFa cells. The present findings substantiate that linalool may act as a photoprotective agent against UVB-induced skin damages.

Highlights

  • The skin is the largest organ of the body and serves as the barrier between the environment and internal cellular milieu which determines its critical function in the preservation of body homeostasis, and eventually organism survival [1]

  • To assess the cytoprotective effect of linalool against ultraviolet -B (UVB) toxicity, we carried out MTT based cytotoxicity assay in human dermal fibroblasts (HDFa) cells

  • We found that UVB irradiation increases the intracellular reactive oxygen species (ROS) production in HDFa cells

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Summary

Introduction

The skin is the largest organ of the body and serves as the barrier between the environment and internal cellular milieu which determines its critical function in the preservation of body homeostasis, and eventually organism survival [1]. Skin possesses strong antioxidant systems which maintain redox homeostasis against oxidative threat in the cellular milieu [3]. Recently Solmonski described the role of neuroendocrine systems such as melatonin/ serotonin in the maintenance of cellular homeostasis in the skin against various environmental stresses [4]. Ultraviolet radiation (UVR) is the prominent environmental agent which continually affects cellular homeostasis in the human skin [5]. Solmonski et al (2014) reported significant alterations in the neuroendocrine system after UVB exposure correlated with carcinogeneic events in the skin cells [6]. It has been well reported that ultraviolet -B (UVB; 285–320 nm) alters skin homeostasis through oxidative imbalance and induces several adverse effects such as erythema, edema, inflammation, photoaging and skin cancer [8]

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