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<p>Environmental pollution caused by fine particulate matter (PM<sub>2.5</sub>) has become increasingly severe. PM<sub>2.5</sub> easily penetrates the skin and causes oxidative damage and inflammatory skin diseases, resulting in skin cell death. In this study, we elucidated the protective effect of <i>Vaccinium oldhamii</i> ethanol extract (VOE) against PM<sub>2.5</sub>-induced oxidative stress, inflammation, and apoptosis in human keratinocytes. The results showed that VOE reversed PM<sub>2.5</sub>-induced decrease in cell viability. VOE strongly inhibited the generation of reactive oxygen species (ROS) by downregulating aryl hydrocarbon receptor (AhR), thereby reducing lipid peroxidation. VOE attenuated PM<sub>2.5</sub>-induced upregulation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling. In addition, VOE markedly reduced PM<sub>2.5</sub>-induced autophagy activation and apoptosis. Overall, VOE prevented PM<sub>2.5</sub>-induced apoptosis by inhibiting ROS generation and mitigating inflammation and autophagy activation. These results suggest the potential of VOE as an effective anti-pollution agent capable of preventing oxidative stress and inflammation caused by PM2.5.</p>

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Protective effects of ethanol extract of Vaccinium oldhamii fruits against fine particulate matter (PM2.5)-induced apoptosis through suppression of oxidative stress and autophagy activation in keratinocytes

  • 期刊论文

  • 发表日期：

    2025年10月29日

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  • Young-Hyeon Lee,
  • Mikyoung You,
  • Eun-Chae Lee,
  • Hyeon-A. Kim

摘要

Environmental pollution caused by fine particulate matter (PM2.5) has become increasingly severe. PM2.5 easily penetrates the skin and causes oxidative damage and inflammatory skin diseases, resulting in skin cell death. In this study, we elucidated the protective effect of Vaccinium oldhamii ethanol extract (VOE) against PM2.5-induced oxidative stress, inflammation, and apoptosis in human keratinocytes. The results showed that VOE reversed PM2.5-induced decrease in cell viability. VOE strongly inhibited the generation of reactive oxygen species (ROS) by downregulating aryl hydrocarbon receptor (AhR), thereby reducing lipid peroxidation. VOE attenuated PM2.5-induced upregulation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling. In addition, VOE markedly reduced PM2.5-induced autophagy activation and apoptosis. Overall, VOE prevented PM2.5-induced apoptosis by inhibiting ROS generation and mitigating inflammation and autophagy activation. These results suggest the potential of VOE as an effective anti-pollution agent capable of preventing oxidative stress and inflammation caused by PM2.5.