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Objective <p>To explore the anti-photoaging properties of salvianolic acid B (Sal B).</p> Methods <p>The optimal photoaging model of human immortalized keratinocytes (HaCaT cells) were constructed by expose to ultraviolet B (UVB) radiation. The cells were divided into control, model and different concentrations of Sal B groups. Cell viability was measured via cell counting kit-8. Subsequently, the levels of oxidative stress, including reactive oxygen species (ROS), hydroxyproline (Hyp), catalase (CAT), and glutathione peroxidase (GSH-Px) were detected using the relevant kits. Silent information regulator 1 (SIRT1) protein level was detected using Western blot. The binding pattern of Sal B and SIRT1 was determined via molecular docking.</p> Results <p>Sal B significantly increased the viability of UVB-irradiated HaCaT cells (<i>P</i>&lt;0.05 or <i>P</i>&lt;0.01). Sal B effectively scavenged the accumulation of ROS induced by UVB (<i>P</i>&lt;0.05 or <i>P</i>&lt;0.01). In addition, Sal B modulated oxidative stress by increasing the intracellular concentrations of Hyp and CAT and the activity of GSH-Px (<i>P</i>&lt;0.05 or <i>P</i>&lt;0.01). The Western blot results revealed a substantial increase in SIRT1 protein levels following Sal B administration (<i>P</i>&lt;0.05). Moreover, Sal B exhibited good binding affinity toward SIRT1, with a docking energy of −7.5 kCal/mol.</p> Conclusion <p>Sal B could improve the repair of photodamaged cells by alleviating cellular oxidative stress and regulating the expression of SIRT1 protein.</p>

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Salvianolic Acid B Exerts Antiphotoaging Effect on Ultraviolet B-Irradiated Human Keratinocytes by Alleviating Oxidative Stress via SIRT1 Protein

  • 期刊论文

  • 发表日期：

    2025年10月24日

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  • Qiao-ju Zhang,
  • Xi Luo,
  • Yu-wen Zheng,
  • Jun-qiao Zheng,
  • Xin-ying Wu,
  • Shu-mei Wang,
  • Jun Shi

摘要

Objective

To explore the anti-photoaging properties of salvianolic acid B (Sal B).

Methods

The optimal photoaging model of human immortalized keratinocytes (HaCaT cells) were constructed by expose to ultraviolet B (UVB) radiation. The cells were divided into control, model and different concentrations of Sal B groups. Cell viability was measured via cell counting kit-8. Subsequently, the levels of oxidative stress, including reactive oxygen species (ROS), hydroxyproline (Hyp), catalase (CAT), and glutathione peroxidase (GSH-Px) were detected using the relevant kits. Silent information regulator 1 (SIRT1) protein level was detected using Western blot. The binding pattern of Sal B and SIRT1 was determined via molecular docking.

Results

Sal B significantly increased the viability of UVB-irradiated HaCaT cells (P<0.05 or P<0.01). Sal B effectively scavenged the accumulation of ROS induced by UVB (P<0.05 or P<0.01). In addition, Sal B modulated oxidative stress by increasing the intracellular concentrations of Hyp and CAT and the activity of GSH-Px (P<0.05 or P<0.01). The Western blot results revealed a substantial increase in SIRT1 protein levels following Sal B administration (P<0.05). Moreover, Sal B exhibited good binding affinity toward SIRT1, with a docking energy of −7.5 kCal/mol.

Conclusion

Sal B could improve the repair of photodamaged cells by alleviating cellular oxidative stress and regulating the expression of SIRT1 protein.