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首页> 外文期刊>Archives of Oral Biology >Bioactive polyphenol antioxidants protect oral fibroblasts from ROS-inducing agents
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Bioactive polyphenol antioxidants protect oral fibroblasts from ROS-inducing agents

机译:具有生物活性的多酚抗氧化剂可保护口腔成纤维细胞免受ROS诱导剂的侵害

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Background: Oxidative damage to soft oral tissues may result from exposure to the chemicals or biochemicals found in teeth-whitening products, dental restorations, tobacco, and alcohol. Our working hypothesis is that oral tissues are susceptible to the toxic effects of stressors such as hydrogen peroxide (H2O2), ethanol (EtOH) and nicotine (Nic), which decrease cell viability/DNA synthesis and elevate reactive oxygen species (ROS). In this study, we investigated specific polyphenols and turmeric derivative antioxidants (AO) in combinations that counteracted the effects of these stressors on cultured oral fibroblast proliferation and ROS production. Methods: Oral fibroblasts were exposed to stressors for 30 min and then treated with 10 -5 M of bioactive AO mixtures [resveratrol, ferulic acid and tetrahydrocurcuminoid (RFT), phloretin, ferulic acid and resveratrol (PFR), phloretin, ferulic acid and tetrahydrocurcuminoid (PFT)] for 24 h. Cell viability and DNA synthesis were monitored using incorporated 3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulphophenyl] -2H-tetrazolium (MTS) and 5-bromo-2-deoxyuridine (BrdU) assays, respectively. Total ROS was measured with dichlorodihydrofluorescein diacetate (H 2DCFDA). Results: Incubation of oral fibroblasts in the stressors for 30 min resulted in a dose-dependent decrease of DNA synthesis and number of viable cells, and an increased total ROS activity. AO treatment counteracted the insults by restoring DNA synthesis levels and cell viability, and decreasing the total ROS activity. Conclusion: The AO combinations of RFT, PFR and PFT protected the oral fibroblasts from the detrimental effects of H 2O2, EtOH and Nic by decreasing total ROS and increasing cell viability and DNA synthesis.
机译:背景:接触牙齿增白产品,牙齿修复剂,烟草和酒精中发现的化学物质或生物化学物质可能导致对口腔软组织的氧化损伤。我们的工作假设是口腔组织易受应激物(如过氧化氢(H2O2),乙醇(EtOH)和尼古丁(Nic))的毒性影响,从而降低细胞活力/ DNA合成并提高活性氧(ROS)。在这项研究中,我们研究了特定的多酚和姜黄衍生物抗氧化剂(AO)的组合,以抵消这些压力源对培养的口腔成纤维细胞增殖和ROS产生的影响。方法:将口腔成纤维细胞暴露于应激下30分钟,然后用10 -5 M的生物活性AO混合物处理[白藜芦醇,阿魏酸和四氢姜黄素(RFT),芦丁,阿魏酸和白藜芦醇(PFR),芦丁,阿魏酸和四氢姜黄素((PFT)] 24小时。使用并入的3- [4,5-二甲基噻唑-2-基] -5- [3-羧基甲氧基苯基] -2- [4-磺苯基] -2H-四唑(MTS)和5-溴-分别进行2-deoxyuridine(BrdU)分析。用二乙酸二氯二氢荧光素(H 2DCFDA)测量总ROS。结果:将口腔成纤维细胞在应激源中孵育30分钟,导致DNA合成和活细胞数量呈剂量依赖性下降,总ROS活性增加。 AO处理通过恢复DNA合成水平和细胞活力并降低总ROS活性来抵消这种损害。结论:RFT,PFR和PFT的AO组合可通过降低总ROS,增加细胞活力和DNA合成来保护口腔成纤维细胞免受H 2O2,EtOH和Nic的有害影响。

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