4.7 Article

Malonic Acid Isolated from Pinus densiflora Inhibits UVB-Induced Oxidative Stress and Inflammation in HaCaT Keratinocytes

Journal

POLYMERS
Volume 13, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/polym13050816

Keywords

Pinus densiflora; malonic acid; UVB; oxidative stress; inflammation

Funding

  1. Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, Forestry, and Fisheries (IPET), through the High Value-added Food Technology Development Program - Ministry of Agriculture, Food, and Rural Affairs (MAFRA) [116010-03-1-CG000]
  2. National Research Foundation (NRF) of Korea - Korean government [NRF-2017R1C1B2005265, 2020R1A2C1100078]
  3. National Research Foundation of Korea [2020R1A2C1100078] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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The study showed that malonic acid (MA) from Pinus densiflora protects against UVB-induced photoaging by reducing ROS levels and inhibiting skin inflammation.
Skin aging is caused by exposure to various external factors. Ultraviolet B (UVB) irradiation induces oxidative stress, photoaging, and inflammation in skin cells. Pinus densiflora Sieb. et Zucc. (red pine) has various antimicrobial and antioxidant activities. However, the anti-inflammatory effects of red pine on skin have rarely been reported. The protective effects of malonic acid (MA) isolated from Pinus densiflora were investigated against UVB-induced damage in an immortalized human keratinocyte cell line (HaCaT). MA increased levels of the antioxidant enzymes superoxide dismutase 1 (SOD-1) and heme oxygenase 1 (HO-1) via activation of nuclear factor-erythroid 2-related factor-2 (Nrf2), resulting in a reduction in UVB-induced reactive oxygen species (ROS) levels. Additionally, the inhibition of ROS increased HaCaT cell survival rate. Thus, MA downregulated the expression of ROS-induced nuclear factor-kappa B, as well as inflammation-related cytokines (interleukin-6, cyclooxygenase-2, and tumor necrosis factor-alpha). Furthermore, MA significantly suppressed the mitogen-activated protein kinase/activator protein 1 signaling pathway and reduced the expression of matrix metalloproteinases (MMPs; MMP-1, MMP-3, and MMP-9). In contrast, MA treatment increased the expression of collagen synthesis regulatory genes (COL1A1 and COL3A1) via regulation of Smad2/3 signal induction through transforming growth factor-beta. In conclusion, MA protected against UVB-induced photoaging via suppression of skin inflammation and induction of collagen biosynthesis.

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