Department of Biomedical Sciences, Texas A&M Health Science Center, Baylor College of Dentistry, Dallas, United States.
Arch Oral Biol. 2012 Dec;57(12):1657-67. doi: 10.1016/j.archoralbio.2012.04.021. Epub 2012 May 28.
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 (H(2)O(2)), 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.
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(2)DCFDA).
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.
The AO combinations of RFT, PFR and PFT protected the oral fibroblasts from the detrimental effects of H(2)O(2), EtOH and Nic by decreasing total ROS and increasing cell viability and DNA synthesis.
口腔软组织的氧化损伤可能是由于接触到牙齿美白产品、牙科修复体、烟草和酒精中的化学物质或生化物质而导致的。我们的工作假设是，口腔组织容易受到过氧化氢 (H2O2)、乙醇 (EtOH) 和尼古丁 (Nic) 等应激源的毒性影响，这些应激源会降低细胞活力/DNA 合成并增加活性氧物种 (ROS)。在这项研究中，我们研究了特定的多酚和姜黄衍生抗氧化剂 (AO) 的组合，这些组合可以对抗这些应激源对培养的口腔成纤维细胞增殖和 ROS 产生的影响。
口腔成纤维细胞暴露于应激源 30 分钟，然后用 10(-5) M 的生物活性 AO 混合物[白藜芦醇、阿魏酸和四氢姜黄素 (RFT)、根皮素、阿魏酸和白藜芦醇 (PFR)、根皮素、阿魏酸和四氢姜黄素 (PFT)]处理 24 小时。通过掺入 3-[4,5-二甲基噻唑-2-基]-5-[3-羧甲氧基苯基]-2-[4-磺苯基]-2H-四唑 (MTS) 和 5-溴-2-脱氧尿苷 (BrdU) 测定法分别监测细胞活力和 DNA 合成。总 ROS 用二氯二氢荧光素二乙酸酯 (H2DCFDA) 测量。
将口腔成纤维细胞在应激源中孵育 30 分钟会导致 DNA 合成和活细胞数量的剂量依赖性减少，以及总 ROS 活性的增加。AO 处理通过恢复 DNA 合成水平和细胞活力以及降低总 ROS 活性来对抗这些损伤。
RFT、PFR 和 PFT 的 AO 混合物通过降低总 ROS 并增加细胞活力和 DNA 合成，保护口腔成纤维细胞免受 H2O2、EtOH 和 Nic 的有害影响。
