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瑞调节了由TEGDMA诱导的矩阵金属蛋白酶表达在人体芽细胞类细胞中
Paula Alejandra Baldión1, Carlos Aldemar Díaz1, Diego Enrique Betancourt1
1Departamento de Salud Oral, Facultad de Odontología, Sede Bogotá, Universidad Nacional de Colombia, Bogotá, Colombia.
Journal of biomedical materials research. Part A
|February 2, 2025
概括
瑞 (MYR) 有效地降低了暴露于树脂单体的人类芽细胞类细胞中反应性氧物种 (ROS) 和矩阵金属蛋白酶 (MMP) 的活性. 这种抗氧化作用可以保护细胞免受损伤,这表明MYR是牙科应用的潜在治疗剂.
科学领域:
- 生物材料科学 生物材料科学
- 细胞生物学 细胞生物学
- 牙科研究 牙科研究
背景情况:
- 矩阵金属蛋白酶 (MMPs),特别是MMP-2和MMP-9,涉及树脂-牙接口降解.
- 牙纸细胞对树脂单体的氧化应激的反应,特别是MMP分泌,需要进一步阐明.
- 像Myricetin (MYR) 和proanthocyanidin (PAC) 这样的抗氧化剂显示出防止细胞外基质降解的潜力.
研究的目的:
- 研究Myricetin (MYR) 对MMP表达和活性的影响.
- 评估MYR对三乙烯糖醇二甲酸盐 (TEGDMA) 诱导的活性氧物种 (ROS) 生成的影响.
- 评估MYR在人类口腔细胞样细胞 (hOLC) 中对TEGDMA诱导的氧化应激的保护潜力.
主要方法:
- 人类的口腔细胞样细胞 (hOLCs) 使用跨井屏障模型暴露于TEGDMA.
- 细胞内ROS水平使用2',7'-二二化素探针进行测量.
- 通过RT-qPCR,ELISA和度测定量出MMP-2和MMP-9的表达和活性,无论是否接受MYR治疗.
主要成果:
- 在hOLC中,TEGDMA暴露显著增加了细胞内ROS和上调的MMP-2和MMP-9mRNA表达.
- 细胞外MMP水平及其激活能力在TEGDMA暴露后24小时显著增加.
- 瑞 (MYR) 治疗有效地降低了ROS的产生,并降低了MMP表达和活性在mRNA和蛋白质水平上的下调.
结论:
- 由于TEGDMA和MMP-2/MMP-9的表达,分泌和激活,ROS增加存在直接相关性.
- 瑞 (MYR) 显示出作为减轻氧化应激和控制MMP活性的治疗策略的巨大潜力.
- MYR通过调节氧还原不平衡和抑制MMP介导的降解,类似于proanthocyanidin (PAC) 对hOLCs提供保护作用.
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