Zhang Shuhong, Chen Yueyue, Qu Liping
Yunnan Botanee Bio-Technology Group Co., Ltd., Yunnan, 650106, China.
Shanghai Jiyan Biomedical Development Co., Ltd., Shanghai, 201702, China.
Sci Rep. 2025 Mar 10;15(1):8260. doi: 10.1038/s41598-025-92559-8.
Chronic inflammation is a critical mechanism contributing to the aging process; however, research specifically addressing chronic inflammation in skin biology remains limited. This study investigates the protective mechanism of Rosa roxburghii Tratt. (RRT) extract against UVB-induced inflammaging. RRT extract effectively reduces the secretion of IL-6, IL-1α, TNF-α, and PGE2 in keratinocytes. Additionally, it attenuates UVB-induced IL-17 pathway activation by downregulating IL-17RA, c-Fos, and c-Jun protein levels, as well as the gene expression of IL-17RA, TRAF6, HSP90, and IKKγ. Co-culturing human foreskin fibroblasts (HFF) with inflammatory factors secreted by UVB-exposed keratinocytes reveals that these factors significantly reduce mitochondrial membrane potential and mitochondrial reactive oxygen species (ROS), thereby promoting aging in HFF. The anti-inflammaging effects of RRT extract are achieved through the reduction of β-galactosidase activity, targeting of the TGF-β1-Smad2/3 signaling pathway, upregulation of COL1A1 expression, and reduction of senescence-associated secretory phenotype secretion. This study provides a novel perspective and robust scientific foundation for exploring mechanisms of skin aging and potential therapeutic interventions.
慢性炎症是导致衰老过程的关键机制；然而，专门针对皮肤生物学中慢性炎症的研究仍然有限。本研究调查了刺梨提取物对紫外线B（UVB）诱导的炎症衰老的保护机制。刺梨提取物可有效减少角质形成细胞中白细胞介素-6（IL-6）、白细胞介素-1α（IL-1α）、肿瘤坏死因子-α（TNF-α）和前列腺素E2（PGE2）的分泌。此外，它通过下调IL-17RA、c-Fos和c-Jun蛋白水平以及IL-17RA、肿瘤坏死因子受体相关因子6（TRAF6）、热休克蛋白90（HSP90）和核因子κB激酶γ（IKKγ）的基因表达来减弱UVB诱导的IL-17途径激活。将人包皮成纤维细胞（HFF）与UVB照射的角质形成细胞分泌的炎症因子共培养发现，这些因子显著降低线粒体膜电位和线粒体活性氧（ROS），从而促进HFF衰老。刺梨提取物的抗炎症衰老作用是通过降低β-半乳糖苷酶活性、靶向转化生长因子-β1（TGF-β1）-Smad2/3信号通路、上调I型胶原蛋白α1（COL1A1）表达以及减少衰老相关分泌表型分泌来实现的。本研究为探索皮肤衰老机制和潜在治疗干预措施提供了新的视角和坚实的科学基础。
