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<p>Platelet-rich plasma (PRP) holds promising prospects for the treatment of skin photoaging. This study aims to unravel the mechanism underlying PRP’s anti-photoaging properties. Partial skin of rats was irradiated with ultraviolet (UV) and injected with PRP, and the skin appearance, pathological state, and aging conditions were determined. Apoptosis, reactive oxygen species (ROS), and collagen levels in skin tissues were detected. HaCaT cells were stimulated with UVB, and the effects of PRP on cells and collagen degradation enzymes were evaluated. Furthermore, the mechanism of the autophagy-NLRP3 inflammasome pathway was explored by treating cells with the autophagy inhibitor 3-MA. Erythema, ulceration, and wrinkles appeared on the skin of rats after being irradiated by UV. PRP could enhance skin tenderness and improve skin pathology and aging. PRP inhibited cell apoptosis, ROS generation, and collagen degradation in skin tissue. PRP elevated UVB-stimulated HaCaT cell activity, reduced oxidative stress, senescence, and MMP-1. Furthermore, 3-MA treatment reversed the inhibition of NLRP3 inflammasome by PRP, suggesting that autophagy mediated the regulation of PRP. To summarize, this study elucidates the regulatory mechanism of PRP on the autophagy-NLRP3 inflammasome pathway in the photoaging. These findings may provide a novel theoretical foundation for the clinical application of PRP.</p>

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Platelet-rich plasma alleviates skin photoaging by activating autophagy and inhibiting inflammasome formation

  • 期刊论文

  • 发表日期：

    2025年1月21日

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  • Zuocai Huang,
  • Zhonghang Gu,
  • Yuanjuan Zeng,
  • Dongxing Zhang

摘要

Platelet-rich plasma (PRP) holds promising prospects for the treatment of skin photoaging. This study aims to unravel the mechanism underlying PRP’s anti-photoaging properties. Partial skin of rats was irradiated with ultraviolet (UV) and injected with PRP, and the skin appearance, pathological state, and aging conditions were determined. Apoptosis, reactive oxygen species (ROS), and collagen levels in skin tissues were detected. HaCaT cells were stimulated with UVB, and the effects of PRP on cells and collagen degradation enzymes were evaluated. Furthermore, the mechanism of the autophagy-NLRP3 inflammasome pathway was explored by treating cells with the autophagy inhibitor 3-MA. Erythema, ulceration, and wrinkles appeared on the skin of rats after being irradiated by UV. PRP could enhance skin tenderness and improve skin pathology and aging. PRP inhibited cell apoptosis, ROS generation, and collagen degradation in skin tissue. PRP elevated UVB-stimulated HaCaT cell activity, reduced oxidative stress, senescence, and MMP-1. Furthermore, 3-MA treatment reversed the inhibition of NLRP3 inflammasome by PRP, suggesting that autophagy mediated the regulation of PRP. To summarize, this study elucidates the regulatory mechanism of PRP on the autophagy-NLRP3 inflammasome pathway in the photoaging. These findings may provide a novel theoretical foundation for the clinical application of PRP.