Linalool prevents oxidative stress activated protein kinases in single UVB-exposed human skin cells

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.

Naringin prevents ultraviolet‐B radiation‐induced oxidative damage and inflammation through activation of peroxisome proliferator‐activated receptor γ in mouse embryonic fibroblast (NIH‐3T3) cells

“…UVB radiation‐induced ROS trigger the activation and phosphorylation of MAPKs signaling pathways mainly leads to oxidative stress and inflammation. Overexpression of MAPKs family members such as ERK‐1, JNK, and p38 regulate downstream factor NF‐κB which is involved in transcriptional activity of several inflammatory proteins such as TNF‐α, IL‐6, IL‐10, and COX‐2 resulted in inflammation and oxidative stress . In this study, naringin prevents the UVB‐induced phosphorylation of ERK‐1, JNK, and p38 in NIH‐3T3.…”

“…In this study, naringin prevents the UVB‐induced phosphorylation of ERK‐1, JNK, and p38 in NIH‐3T3. Similarly, linalool monoterpenoid prevents UVB‐induced phosphorylation of ERK‐1, JNK, and p38 in HDFa cells …”

“…hOGG1‐modified comet assay was used to detect 8‐deoxyguanosines (8‐OxoG) in UVB‐irradiated NIH‐3T3 cell lines . A layer of 1% NMPA was prepared on microscope slides.…”

“…Supernatants were collected and it was used for Western blot analysis. Preparation of cytosolic and nuclear fractions were followed as described by Gunaseelan et al Proteins were subjected to 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to polyvinylidene difluoride (PVDF) membranes for the analysis of ERK‐1, JNK, p38, TNF‐α, IL‐6, IL‐10, COX‐2, NF‐κB, and PPARγ. Membranes were washed with tris‐buffered saline (TBS) containing 0.05% Tween‐20 (TBST), and were then blocked for 1 hour in TBS containing 3% BSA.…”

“…UVB exposure to skin affects the cellular endogenous antioxidant enzymes in the skin, which is responsible for cellular signaling modification and oxidative stress . UVB radiation‐induced oxidative stress is caused by overexpression of mitogen‐activated protein kinases (MAPKs) families which include extracellular signal‐regulated kinases (ERK1/2), c‐Jun N‐terminal kinase (JNK), and p38 kinases .…”