Potential Protective Effects of Cerium Oxide Nanoparticles on Ultraviolet-B Irradiated Fibroblast Cells.

IF 1.8 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Reza Fardid, Mansooreh Mostafavi Mendi, Gholamhassan Haddadi, Mohammad Ali Takhshid
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引用次数: 0

Abstract

Increased environmental ultraviolet-B (UVB) exposure stimulates reactive oxygen species (ROS) overproduction, disrupts cellular redox balance, and contributes to skin disorders. Antioxidants inhibit autoxidation by neutralizing or suppressing free radicals. Certain nanomaterials, like cerium oxide nanoparticles (CNPs), function as antioxidants under specific conditions. Through their redox and catalytic properties, CNPs scavenge ROS, mitigate oxidative damage, and may help prevent skin injuries. While most research targets ionizing radiation, studies exploring CNPs under non-ionizing UVB remain limited. To address this, the study evaluates their photochemoprotective effects in UVB-exposed L929 fibroblasts. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), cupric ion reducing antioxidant capacity (CUPRAC), dichloro-dihydro-fluorescein diacetate (DCFH-DA), and annexin V/propidium iodide (annexin V/PI) assays were used to evaluate cell viability, oxidative stress, and apoptosis. Cell viability was assessed using the MTT assay at CNP concentrations of 10, 50, and 100 μM and UVB intensities of 150-900 mJ/cm², selected based on prior physiologically relevant in vitro studies. At 600 mJ/cm² UVB, cell viability decreased by 45% (MTT assay). Treatment with 50 μM CNP significantly increased total antioxidant capacity relative to untreated controls (CUPRAC assay, p = 0.0018). CNP and UVB effects on ROS production and apoptosis were evaluated separately and in combination using DCFH-DA and annexin V/PI assays. Results show that pretreatment with CNPs before UVB radiation impedes cell apoptosis and reduces ROS, suggesting that CNPs mitigate UVB-induced oxidative damage in L929 cells by restoring oxidative balance through their redox activity and ROS-scavenging properties. These findings indicate CNP-based interventions may offer therapeutic strategies against UVB-induced skin and related disorders.

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氧化铈纳米颗粒对紫外线照射成纤维细胞的潜在保护作用。
增加的环境紫外线b (UVB)暴露刺激活性氧(ROS)过量产生,破坏细胞氧化还原平衡,并导致皮肤疾病。抗氧化剂通过中和或抑制自由基来抑制自氧化。某些纳米材料,如氧化铈纳米颗粒(CNPs),在特定条件下具有抗氧化剂的功能。通过其氧化还原和催化特性,CNPs清除ROS,减轻氧化损伤,并可能有助于预防皮肤损伤。虽然大多数研究以电离辐射为目标,但在非电离UVB下探索CNPs的研究仍然有限。为了解决这个问题,本研究评估了它们在uvb暴露的L929成纤维细胞中的光化学保护作用。采用3-(4,5 -二甲基噻唑-2-酰基)- 2,5 -二苯基溴化四唑(MTT)、铜离子还原抗氧化能力(CUPRAC)、二氯-二氢荧光素双乙酸酯(DCFH-DA)和膜联蛋白V/碘化丙啶(膜联蛋白V/PI)检测来评估细胞活力、氧化应激和凋亡。在CNP浓度为10、50和100 μM, UVB强度为150-900 mJ/cm²的条件下,使用MTT法评估细胞活力,这些强度是根据先前的生理相关体外研究选择的。在600 mJ/cm²UVB下,细胞活力下降45% (MTT测定)。与未处理的对照组相比,50 μM CNP处理显著提高了总抗氧化能力(CUPRAC测定,p = 0.0018)。通过DCFH-DA和膜联蛋白V/PI检测分别评估CNP和UVB对ROS产生和细胞凋亡的影响。结果表明,在UVB照射前使用CNPs预处理可抑制细胞凋亡并减少ROS,表明CNPs通过其氧化还原活性和清除ROS的特性恢复氧化平衡,从而减轻UVB诱导的L929细胞氧化损伤。这些发现表明,基于cnp的干预措施可能提供针对uvb诱导的皮肤和相关疾病的治疗策略。
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来源期刊
CiteScore
3.60
自引率
0.00%
发文量
0
期刊介绍: The International Journal of Molecular and Cellular Medicine (IJMCM) is a peer-reviewed, quarterly publication of Cellular and Molecular Biology Research Center (CMBRC), Babol University of Medical Sciences, Babol, Iran. The journal covers all cellular & molecular biology and medicine disciplines such as the genetic basis of disease, biomarker discovery in diagnosis and treatment, genomics and proteomics, bioinformatics, computer applications in human biology, stem cells and tissue engineering, medical biotechnology, nanomedicine, cellular processes related to growth, death and survival, clinical biochemistry, molecular & cellular immunology, molecular and cellular aspects of infectious disease and cancer research. IJMCM is a free access journal. All open access articles published in IJMCM are distributed under the terms of the Creative Commons Attribution CC BY. The journal doesn''t have any submission and article processing charges (APCs).
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