Background: The exposure of the human skin to particulate matter 2.5 (PM_2.5) results in adverse health outcomes, such as skin aging, wrinkle formation, pigment spots, and atopic dermatitis. It has previously been shown that rosmarinic acid (RA) can protect keratinocytes from ultraviolet B radiation by enhancing cellular antioxidant systems and reducing oxidative damage; however, its protective action against the adverse effects of PM_2.5 on skin cells remains unclear. Therefore, in this study, we explored the mechanism underlying the protective effects of RA against PM_2.5-mediated oxidative stress in HaCaT keratinocytes./nMethods: HaCaT keratinocytes were pretreated with RA and exposed to PM_2.5. Thereafter, reactive oxygen species (ROS) production, protein carbonylation, lipid peroxidation, DNA damage, and cellular apoptosis were investigated using various methods, including confocal microscopy, western blot analysis, and flow cytometry./nResults: RA significantly inhibited PM_2.5-induced lipid peroxidation, protein carbonylation, DNA damage, increases in intracellular Ca²⁺ level, and mitochondrial depolarization. It also significantly attenuated PM_2.5-induced apoptosis by downregulating Bcl-2-associated X, cleaved caspase-9, and cleaved caspase-3 protein levels, while upregulating B-cell lymphoma 2 protein level. Further, our results indicated that PM_2.5-induced apoptosis was associated with the activation of the mitogen-activated protein kinase (MAPK) signaling pathway and that MAPK inhibitors as well as RA exhibited protective effects against PM_2.5-induced apoptosis./nConclusion: RA protected HaCaT cells from PM_2.5-induced apoptosis by lowering oxidative stress.

中文翻译：

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迷迭香酸保护皮肤角质形成细胞免受颗粒物 2.5 诱导的细胞凋亡

背景：人体皮肤暴露于颗粒物 2.5 (PM _2.5 ) 会导致不良健康结果，例如皮肤老化、皱纹形成、色素斑和特应性皮炎。此前已有研究表明，迷迭香酸（RA）可以通过增强细胞抗氧化系统和减少氧化损伤来保护角质形成细胞免受紫外线B辐射；_{然而，其针对 PM 2.5}对皮肤细胞不利影响的保护作用仍不清楚。_{因此，在本研究中，我们探讨了 RA 对 HaCaT 角质形成细胞中 PM 2.5}介导的氧化应激的保护作用的机制。/n方法：用 RA 预处理 HaCaT 角质形成细胞并暴露于 PM _2.5。此后，使用各种方法研究活性氧 (ROS) 产生、蛋白质羰基化、脂质过氧化、DNA 损伤和细胞凋亡，包括共聚焦显微镜、蛋白质印迹分析和流式细胞术。/n 结果： RA 显着抑制 PM _2.5 -诱导脂质过氧化、蛋白质羰基化、DNA 损伤、细胞内 Ca ²⁺水平增加和线粒体去极化。它还通过下调 Bcl-2 相关 X、cleaved caspase-9 和 cleaved caspase-3 蛋白水平，同时上调 B 细胞淋巴瘤 2 蛋白水平，显着减弱PM _{2.5诱导的细胞凋亡。}此外，我们的结果表明，PM _2.5诱导的细胞凋亡与丝裂原激活蛋白激酶 (MAPK) 信号通路的激活有关，MAPK 抑制剂以及 RA 对 PM _2.5诱导的细胞凋亡具有保护作用。/n 结论： RA 通过降低氧化应激来保护 HaCaT 细胞免受 PM _2.5诱导的细胞凋亡。