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<p>Ultraviolet B (UVB) exposure represents a significant environmental pathogenic factor of skin photodamage. Kaempferol (KFL) is a natural polyphenolic compound with significant antioxidant properties, but its effects on photodamage and associated molecular pathways remain incompletely elucidated. This study investigates the function of KFL in UVB-induced photodamage and its related mechanisms. Prior to UVB exposure, Human Immortalized Epidermal Cells (HaCaT cells) underwent KFL treatment. The shielding capacity of KFL against UVB-mediated photodamage in HaCaT cells was assessed by analyzing cell damage indicators, oxidative stress levels, and inflammation. Furthermore, the expression of Phosphoinositide3-kinase/Protein kinase B/Nuclear factor erythroid 2-related factor 2(PI3K/AKT/Nrf2)-related proteins was analyzed, and the use of the PI3K-specific inhibitor LY294002 was employed to verify whether the photoprotective effects of KFL in HaCaT cells occur via the PI3K/AKT/Nrf2 signaling cascade. Our results suggest that KFL markedly alleviated UVB-induced HaCaT cell damage, reactive oxygen species (ROS) production, and inflammation levels. Additionally, KFL appeared to upregulate PI3K/AKT/Nrf2-related protein expression, while the use of LY294002 partially reversed these KFL-induced effects. This investigation indicates that KFL may exert protective effects against UVB-induced photodamage by activating the PI3K/AKT/Nrf2 pathway, enhancing the endogenous defense mechanisms in HaCaT cells, and reducing UVB-induced ROS generation.</p>

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Kaempferol attenuates UVB-induced photodamage by activating the PI3K/AKT/Nrf2 pathway in HaCaT cells

  • 期刊论文

  • 发表日期：

    2025年12月19日

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  • Liang Chen,
  • Ayidana Ayoujiang,
  • Shuning Feng,
  • Yuxin Zhang,
  • Wei Wang,
  • Dong Dong,
  • Heng Wang,
  • Bo Bi,
  • Tianyi Liu

摘要

Ultraviolet B (UVB) exposure represents a significant environmental pathogenic factor of skin photodamage. Kaempferol (KFL) is a natural polyphenolic compound with significant antioxidant properties, but its effects on photodamage and associated molecular pathways remain incompletely elucidated. This study investigates the function of KFL in UVB-induced photodamage and its related mechanisms. Prior to UVB exposure, Human Immortalized Epidermal Cells (HaCaT cells) underwent KFL treatment. The shielding capacity of KFL against UVB-mediated photodamage in HaCaT cells was assessed by analyzing cell damage indicators, oxidative stress levels, and inflammation. Furthermore, the expression of Phosphoinositide3-kinase/Protein kinase B/Nuclear factor erythroid 2-related factor 2(PI3K/AKT/Nrf2)-related proteins was analyzed, and the use of the PI3K-specific inhibitor LY294002 was employed to verify whether the photoprotective effects of KFL in HaCaT cells occur via the PI3K/AKT/Nrf2 signaling cascade. Our results suggest that KFL markedly alleviated UVB-induced HaCaT cell damage, reactive oxygen species (ROS) production, and inflammation levels. Additionally, KFL appeared to upregulate PI3K/AKT/Nrf2-related protein expression, while the use of LY294002 partially reversed these KFL-induced effects. This investigation indicates that KFL may exert protective effects against UVB-induced photodamage by activating the PI3K/AKT/Nrf2 pathway, enhancing the endogenous defense mechanisms in HaCaT cells, and reducing UVB-induced ROS generation.