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

Srithar Gunaseelan1, Agilan Balupillai1, Kanimozhi Govindasamy1,2

  • 1Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, India.

Plos One
|May 4, 2017
PubMed

Insights

Linalool, a natural compound, protects human skin cells from UVB damage by preventing oxidative stress and regulating key signaling pathways like MAPK and NF-κB. It acts as a potential photoprotective agent against sun-induced skin harm.

Area of Science:

  • Dermatology
  • Biochemistry
  • Molecular Biology

Background:

  • Ultraviolet-B (UVB) radiation induces cellular damage via oxidative imbalance and signaling pathway activation.
  • Mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) pathways are critical in UVB-induced skin responses.
  • Human dermal fibroblasts (HDFa) are susceptible to UVB-induced damage, including DNA lesions and inflammation.

Purpose of the Study:

  • To investigate the protective effects of linalool against UVB-induced oxidative stress and signaling pathway activation in HDFa cells.
  • To determine if linalool can prevent DNA damage and modulate inflammatory responses triggered by UVB radiation.
  • To evaluate linalool's potential as a photoprotective agent.

Main Methods:

  • HDFa cells were treated with linalool (30 μM) and exposed to UVB radiation (20 mJ/cm²).
  • Assays were performed to measure antioxidant enzyme activity, 8-deoxyguanosine and cyclobutane pyrimidine (CPD) formation, and reactive oxygen species (ROS) levels.
  • Western blotting and other molecular techniques were used to assess MAPK (ERK1, JNK, p38) and NF-κB (p65, IκBa) signaling activation.
  • Expression levels of inflammatory cytokines (TNF-α, IL6, IL-10) and matrix metalloproteinases (MMP-2, MMP-9) were analyzed.

Main Results:

  • Linalool treatment prevented the loss of antioxidant enzyme activities and reduced UVB-induced ROS formation in HDFa cells.
  • Linalool significantly inhibited UVB-mediated 8-deoxyguanosine formation (oxidative DNA damage) but had less effect on CPD formation.
  • Linalool suppressed UVB-induced phosphorylation of MAPK proteins (ERK1, JNK, p38) and inhibited NF-κB/p65 activation by upregulating IκBa.
  • The expression of UVB-induced TNF-α, IL6, IL-10, MMP-2, and MMP-9 was modulated by linalool.

Conclusions:

  • Linalool effectively protects human skin cells from UVB-induced oxidative damage by preventing ROS generation and restoring oxidative balance.
  • Linalool modulates critical UVB-responsive signaling pathways, including MAPK and NF-κB, thereby mitigating downstream inflammatory effects.
  • These findings support the potential of linalool as a natural photoprotective agent against UVB-induced skin damage.