Departamento de Ciencias Químico Biológicas, Instituto de Ciencias Biomédicas, Universidad Autónoma de Ciudad Juárez, PRONAF y Estocolmo s/n, 32310, Juárez, Mexico.
X-ray and Infrared Microspectroscopy Beamline ID21, European Synchrotron Radiation Facility, 71 avenue des Martyrs, 38000, Grenoble, France.
Spectrochim Acta A Mol Biomol Spectrosc. 2020 Feb 15;227:117570. doi: 10.1016/j.saa.2019.117570. Epub 2019 Oct 20.
Phenolic compounds (PC) have been proposed as natural antioxidant agents that protect cells against oxidative stress-related diseases. Nonetheless, their low bioavailability forecasts controversy about mechanisms on their in vivo scavenging activity against reactive oxygen species (ROS). It has been proposed that PC reduce directly ROS concentration. An alternative or complementary action of PC could be the activation of the cell's antioxidant pathway, involving the regulation of gene expression, like that initiated by the Nrf2 transcription factor. To date there is not enough experimental data to support or discard this possibility. In the present study, we evaluated the use of several PC to prevent peroxidation of macromolecules and to elicit the activation of the Nrf2 transcription factor in HO-stresed IEC-6 enterocytic cell line. Synchrotron microspectroscopy demonstrated that PC compounds protected proteins, lipids and nucleic acids against oxidation induced by HO. Immunofluorescence results showed that treatment with quercetin (Qc), catechin (Cat) and capsaicin (Cap) induced the translocation of Nrf2 into the nucleus, at the same level as did HO treatment, thus mimicking the action of the endogenous cell response to peroxidation. Even though the detailed mechanism still needs to be elucidated, we demonstrated the activation of Nrf2 by PCs in response to oxidative stress.
酚类化合物 (PC) 已被提议作为天然抗氧化剂，可保护细胞免受与氧化应激相关的疾病的侵害。尽管如此，其生物利用度低的情况预测了其在体内清除活性氧 (ROS) 方面的机制存在争议。有人提出 PC 可以直接降低 ROS 浓度。PC 的另一种或补充作用可能是激活细胞的抗氧化途径，包括基因表达的调节，就像由 Nrf2 转录因子引发的那样。迄今为止，没有足够的实验数据来支持或排除这种可能性。在本研究中，我们评估了几种 PC 的使用，以防止大分子的过氧化，并在 HO 应激的 IEC-6 肠细胞系中引发 Nrf2 转录因子的激活。同步辐射微光谱表明，PC 化合物可保护蛋白质、脂质和核酸免受 HO 诱导的氧化。免疫荧光结果表明，与 HO 处理相同，槲皮素 (Qc)、儿茶素 (Cat) 和辣椒素 (Cap) 处理诱导 Nrf2 向核内易位，从而模拟了细胞对过氧化的内源性反应的作用。尽管详细的机制仍需要阐明，但我们证明了 PCs 在应对氧化应激时激活 Nrf2。
