Department of Analytical Chemistry, Medical University of Bialystok, Kilinskiego 1, 15-069 Bialystok, Poland.
Mass Spectrometry Centre, LAQV-REQUIMTE, Department of Chemistry, University of Aveiro, Santiago University Campus, 3810-193 Aveiro, Portugal.
Int J Mol Sci. 2023 Sep 20;24(18):14323. doi: 10.3390/ijms241814323.
Ultraviolet B (UVB) radiation induces oxidative stress in skin cells, generating reactive oxygen species (ROS) and perturbing enzyme-mediated metabolism. This disruption is evidenced with elevated concentrations of metabolites that play important roles in the modulation of redox homeostasis and inflammatory responses. Thus, this research sought to determine the impacts of the lipid extract derived from the microalgae on phospholipid metabolic processes in keratinocytes subjected to UVB exposure. UVB-irradiated keratinocytes were treated with the microalgae extract. Subsequently, analyses were performed on cell lysates to ascertain the levels of phospholipid/free fatty acids (GC-FID), lipid peroxidation byproducts (GC-MS), and endocannabinoids/eicosanoids (LC-MS), as well as to measure the enzymatic activities linked with phospholipid metabolism, receptor expression, and total antioxidant status (spectrophotometric methods). The extract from microalgae, by diminishing the activities of enzymes involved in the synthesis of endocannabinoids and eicosanoids (PLA2/COX1/2/LOX), augmented the concentrations of anti-inflammatory and antioxidant polyunsaturated fatty acids (PUFAs), namely DHA and EPA. These concentrations are typically diminished due to UVB irradiation. As a consequence, there was a marked reduction in the levels of pro-inflammatory arachidonic acid (AA) and associated pro-inflammatory eicosanoids and endocannabinoids, as well as the expression of CB1/TRPV1 receptors. The microalgal extract also mitigated the increase in lipid peroxidation byproducts, specifically MDA in non-irradiated samples and 10-F4t-NeuroP in both control and post-UVB exposure. These findings indicate that the lipid extract derived from , by mitigating the deleterious impacts of UVB radiation on keratinocyte phospholipids, assumed a pivotal role in reinstating intracellular metabolic equilibrium.
紫外线 B(UVB)辐射会导致皮肤细胞产生氧化应激,生成活性氧(ROS)并扰乱酶介导的新陈代谢。这种破坏表现在代谢物浓度升高,这些代谢物在调节氧化还原平衡和炎症反应中起着重要作用。因此,本研究旨在确定从微藻中提取的脂质提取物对暴露于 UVB 下的角质形成细胞中磷脂代谢过程的影响。用微藻提取物处理 UVB 照射的角质形成细胞。随后,对细胞裂解物进行分析,以确定磷脂/游离脂肪酸(GC-FID)、脂质过氧化产物(GC-MS)和内源性大麻素/类二十烷酸(LC-MS)的水平,以及测量与磷脂代谢、受体表达和总抗氧化状态(分光光度法)相关的酶活性。微藻提取物通过降低参与内源性大麻素和类二十烷酸合成的酶的活性(PLA2/COX1/2/LOX),增加了抗炎和抗氧化多不饱和脂肪酸(PUFAs)的浓度,即 DHA 和 EPA。这些浓度通常因 UVB 照射而降低。因此,促炎花生四烯酸(AA)及其相关促炎类二十烷酸和内源性大麻素的水平以及 CB1/TRPV1 受体的表达显著降低。微藻提取物还减轻了脂质过氧化产物的增加,特别是非照射样品中的 MDA 和对照和 UVB 照射后样品中的 10-F4t-NeuroP。这些发现表明,从 中提取的脂质提取物通过减轻 UVB 辐射对角质形成细胞膜磷脂的有害影响,在恢复细胞内代谢平衡方面发挥了关键作用。