Huang Zuocai, Gu Zhonghang, Zeng Yuanjuan, Zhang Dongxing
Department of Emergency Medicine, Dongshan Hospital, Meijiang District, Meizhou, 514011, Guangdong, China.
Department of Dermatology, Dongshan Hospital, Guofengyuan Building, Xuezi Avenue, Meijiang District, Meizhou, 514011, Guangdong, China.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jan 21. doi: 10.1007/s00210-025-03800-0.
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.
富血小板血浆（PRP）在皮肤光老化治疗方面具有广阔前景。本研究旨在揭示PRP抗光老化特性的潜在机制。对大鼠部分皮肤进行紫外线（UV）照射并注射PRP，然后测定皮肤外观、病理状态和老化情况。检测皮肤组织中的细胞凋亡、活性氧（ROS）和胶原蛋白水平。用UVB刺激HaCaT细胞，评估PRP对细胞和胶原蛋白降解酶的影响。此外，通过用自噬抑制剂3-MA处理细胞来探索自噬-NLRP3炎性小体途径的机制。UV照射后大鼠皮肤出现红斑、溃疡和皱纹。PRP可增强皮肤敏感性，改善皮肤病理和老化情况。PRP抑制皮肤组织中的细胞凋亡、ROS生成和胶原蛋白降解。PRP提高UVB刺激的HaCaT细胞活性，降低氧化应激、衰老和基质金属蛋白酶-1（MMP-1）水平。此外，3-MA处理逆转了PRP对NLRP3炎性小体的抑制作用，表明自噬介导了PRP的调节作用。综上所述，本研究阐明了PRP在光老化中对自噬-NLRP3炎性小体途径的调节机制。这些发现可能为PRP的临床应用提供新的理论基础。
