Wang Ben, Dong Jie, Liu Fang
Dermatology Department, Beijing Chaoyang Hospital Affiliated to Capital Medical University, 100020 Beijing, China.
Discov Med. 2025 Jan;37(192):193-201. doi: 10.24976/Discov.Med.202537192.16.
Ultraviolet (UV) radiation-induced photoaging is a multifaceted biological process. Fruit acids have shown promise in combating photoaging. This study aims to investigate the mechanisms underlying the protective effects of fruit acids on UV-induced skin photoaging.
Initially, we induced skin photoaging in rats through UV irradiation. Subsequently, the model group received glycolic acid treatment. The reparative effects of glycolic acid on skin tissue morphology and structure were assessed using Hematoxylin-eosin (HE) staining. The influence of glycolic acid on oxidative stress indicators (Superoxide Dismutase (SOD), Glutathione Peroxidase (GSH-Px), Malondialdehyde (MDA), Catalase (CAT)) and levels of cellular inflammatory factors (Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), IL-1β, Interferon-gamma (IFN-γ)) in photoaged skin was evaluated via Enzyme-Linked Immunosorbent Assay (ELISA). Additionally, alterations in collagen expression and levels of proteins associated with the Phosphoinositide 3-kinase/Protein Kinase B (PI3K/Akt) and Nuclear Factor kappa B (NF-κB) signaling pathways were determined through Western blot analysis.
Compared to the model group, the fruit group exhibited a decrease in the thickness of the skin epidermal keratinization layer, an increase in dermal thickness, and more vigorous cortical secretion. Moreover, compared with the model group, the fruit group showed significant increases in SOD activity, CAT, GSH-Px, Collagen I, Collagen III, Collagen VII, and elastin. Conversely, levels of MDA, IL-6, IL-1β, IFN-γ, and TNF-α were lower in the fruit acid group than in the model group. Additionally, fruit acid treatment inhibited the phosphorylation levels of PI3K, Akt, and p65 induced by UV.
Fruit acid demonstrates the ability to diminish the oxidative stress and inflammatory responses in skin photoaging rat models, thereby facilitating collagen recovery and ameliorating symptoms of skin photoaging. Its potential mechanism may entail the inhibition of the activation of the PI3K/Akt and NF-κB signaling pathways.
紫外线（UV）辐射诱导的光老化是一个多方面的生物学过程。果酸已显示出对抗光老化的潜力。本研究旨在探讨果酸对紫外线诱导的皮肤光老化保护作用的潜在机制。
首先，我们通过紫外线照射诱导大鼠皮肤光老化。随后，模型组接受乙醇酸治疗。使用苏木精-伊红（HE）染色评估乙醇酸对皮肤组织形态和结构的修复作用。通过酶联免疫吸附测定（ELISA）评估乙醇酸对光老化皮肤中氧化应激指标（超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）、过氧化氢酶（CAT））和细胞炎症因子水平（白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、IL-1β、干扰素-γ（IFN-γ））的影响。此外，通过蛋白质印迹分析确定胶原蛋白表达以及与磷酸肌醇3-激酶/蛋白激酶B（PI3K/Akt）和核因子κB（NF-κB）信号通路相关的蛋白质水平的变化。
与模型组相比，果酸组皮肤表皮角质化层厚度降低，真皮厚度增加，皮质分泌更旺盛。此外，与模型组相比，果酸组的SOD活性、CAT、GSH-Px、I型胶原蛋白、III型胶原蛋白、VII型胶原蛋白和弹性蛋白显著增加。相反，果酸组中MDA、IL-6、IL-1β、IFN-γ和TNF-α的水平低于模型组。此外，果酸治疗抑制了紫外线诱导的PI3K、Akt和p65的磷酸化水平。
果酸显示出减轻皮肤光老化大鼠模型中氧化应激和炎症反应的能力，从而促进胶原蛋白恢复并改善皮肤光老化症状。其潜在机制可能涉及抑制PI3K/Akt和NF-κB信号通路的激活。
