Supplementary Material for: Walnuts (Seeds of <b><i>Juglandis</i></b> <b><i>sinensis</i></b> L.) Protect Human Epidermal Keratinocytes against UVB-Induced Mitochondria-Mediated Apoptosis through Upregulation of ROS Elimination Pathways

<b><i>Purpose:</i></b> Ultraviolet (UV) light from sunlight is an important environmental factor causing hazardous health effects, including various skin disorders. UV irradiation downregulates reactive oxygen species (ROS) elimination pathways, thereby promoting the production of ROS, which are implicated in mitochondria-mediated apoptosis. Walnuts, the seeds of <i>Juglandis</i><i>sinensis</i> L., are a highly nutritious food and have been shown to have a number of pharmacological activities. To our knowledge, no study on the protective effects of walnuts on human epidermal keratinocytes has been reported previously. Here, we investigated the protective effects of walnuts against UVB (50 mJ/cm²) -induced mitochondria-mediated apoptosis. <b><i>Procedures and Results:</i></b> Walnuts significantly and dose-dependently reduced UVB-induced apoptotic toxicity by lactate dehydrogenase assay kit. Walnuts decreased mitochondrial dysfunction, B-cell lymphoma 2 (Bcl-2)-associated X (Bax) protein levels, and cytochrome c release from mitochondria, while increasing Bcl-2 protein levels using immunofluorescence, Western blot, or kit analysis. Moreover, walnuts inhibited caspase-3 activity, indicating an inhibition of the apoptotic cascade, and induced the expression of heme oxygenase and NAD(P)H dehydrogenase via NF-E2-related factor-2 activation using immunofluorescence or Western blot analysis. <b><i>Conclusion:</i></b> Together, these results demonstrate that walnuts can protect human epidermal keratinocytes against UVB-induced mitochondria-mediated apoptosis by regulating ROS elimination pathways.

<b><i>研究目的：</i></b> 日光中的紫外线（Ultraviolet, UV）是引发包括多种皮肤疾病在内的有害健康效应的重要环境因素。紫外线辐射会下调活性氧（reactive oxygen species, ROS）清除通路，进而促进活性氧的生成，而活性氧与线粒体介导的细胞凋亡密切相关。胡桃为<i>Juglandis sinensis</i> L.的种子，是一种营养丰富的食品，且已被证实具有多种药理活性。据现有文献报道，尚未见关于胡桃对人表皮角质形成细胞保护作用的相关研究。本研究旨在探究胡桃对50 mJ/cm² UVB诱导的线粒体介导细胞凋亡的保护效应。<b><i>实验方法与结果：</i></b> 经乳酸脱氢酶检测试剂盒检测，胡桃可显著且呈剂量依赖性地降低UVB诱导的细胞凋亡毒性。经免疫荧光、蛋白质印迹（Western blot）法或相关试剂盒检测证实，胡桃可改善线粒体功能障碍，下调B细胞淋巴瘤2（B-cell lymphoma 2, Bcl-2）相关X蛋白（Bax）的表达水平，减少细胞色素c（cytochrome c）从线粒体中的释放，同时上调Bcl-2蛋白的表达。此外，经免疫荧光或蛋白质印迹法检测可知，胡桃可抑制半胱氨酸天冬氨酸蛋白酶-3（caspase-3）的活性，从而阻断细胞凋亡级联反应；同时通过激活核因子红细胞2相关因子2（NF-E2-related factor-2, Nrf2）通路，诱导血红素加氧酶（heme oxygenase）及NAD(P)H脱氢酶（NAD(P)H dehydrogenase）的表达。<b><i>研究结论：</i></b> 综上，上述结果表明，胡桃可通过调控活性氧清除通路，使人表皮角质形成细胞抵御UVB诱导的线粒体介导细胞凋亡。

搜集汇总

背景与挑战

背景概述

该数据集为一项研究的补充材料，聚焦于核桃（Juglandis sinensis L.种子）对人类表皮角质细胞在UVB诱导下线粒体介导凋亡的保护作用。数据集通过实验数据展示了核桃如何剂量依赖性地减少UVB引起的细胞凋亡，并调节ROS清除途径（如激活NF-E2相关因子-2），从而抑制线粒体功能障碍和凋亡级联反应。