关键词: AMPK Autophagy Photoaging ROS Resveratrol UVA

Mesh : Resveratrol / pharmacology Skin Aging / drug effects radiation effects Fibroblasts / drug effects radiation effects metabolism Autophagy / drug effects radiation effects Animals Ultraviolet Rays / adverse effects Humans Male AMP-Activated Protein Kinases / metabolism Mice Skin / drug effects radiation effects pathology metabolism Stilbenes / pharmacology Signal Transduction / drug effects Reactive Oxygen Species / metabolism Antioxidants / pharmacology Apoptosis / drug effects radiation effects

来  源:   DOI:10.1007/s10522-024-10099-6   PDF(Pubmed)

Abstract:
Skin photoaging is mostly caused by ultraviolet A (UVA), although active medications to effectively counteract UVA-induced photoaging have not yet been created. Resveratrol, a naturally occurring polyphenol found in the skin of grapes, has been shown to have various biological functions such as anti-inflammatory and antioxidant characteristics. However, the role of resveratrol in UVA-induced photoaging has not been clarified. We investigated the mechanism of action of resveratrol by UVA irradiation of human skin fibroblasts (HSF) and innovatively modified a mouse model of photoaging. The results demonstrated that resveratrol promoted AMP-activated protein kinase (AMPK) phosphorylation to activate autophagy, reduce reactive oxygen species (ROS) production, inhibit apoptosis, and restore normal cell cycle to alleviate UVA-induced photoaging. In addition, subcutaneous injection of resveratrol not only improved the symptoms of roughness, erythema, and increased wrinkles in the skin of UVA photodamaged mice, but also alleviated epidermal hyperkeratosis and hyperpigmentation, reduced inflammatory responses, and inhibited collagen fiber degradation. In conclusion, our studies proved that resveratrol can treat UVA-induced photoaging and elucidated the possible molecular mechanisms involved, providing a new therapeutic strategy for future anti-aging.
摘要:
皮肤光老化主要是由紫外线A(UVA)引起的,尽管目前还没有产生有效对抗UVA诱导的光老化的活性药物。白藜芦醇,一种天然存在于葡萄皮中的多酚,已被证明具有多种生物学功能,例如抗炎和抗氧化特性。然而,白藜芦醇在UVA诱导的光老化中的作用尚未阐明。我们研究了白藜芦醇通过UVA照射人皮肤成纤维细胞(HSF)的作用机制,并创新性地修改了光老化的小鼠模型。结果表明,白藜芦醇可促进AMP激活蛋白激酶(AMPK)磷酸化激活自噬,减少活性氧(ROS)的产生,抑制细胞凋亡,恢复正常的细胞周期以减轻UVA诱导的光老化。此外,皮下注射白藜芦醇不仅改善了粗糙的症状,红斑,UVA光损伤小鼠皮肤皱纹增加,但也减轻了表皮角化过度和色素沉着,减少炎症反应,抑制胶原纤维降解。总之,我们的研究证明白藜芦醇可以治疗UVA诱导的光老化,并阐明了其中可能的分子机制,为未来抗衰老提供新的治疗策略。
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