Departments of Physiology, School of Medicine, Sivas Cumhuriyet University, 58140 Sivas, Turkey.
Department of Biochemistry, Faculty of Pharmacy, Sivas Cumhuriyet University, 58140 Sivas, Turkey.
Brain Res. 2024 Dec 1;1844:149175. doi: 10.1016/j.brainres.2024.149175. Epub 2024 Aug 19.
Recent investigations indicate that tannic acid is associated with a decrease in oxidative damage. Growing evidence supports the protective effects of tannic acid on the central nervous system (CNS). However, uncertainties persist regarding its influence on hydrogen peroxide (HO)-triggered oxidative impairment in nerve cells and its interaction with apoptosis. Hence, the objective of this work was to examine the neuroprotective impact of tannic acid on SH-SY5Y cell impairment following HO-induced oxidative stress, particularly concerning apoptotic pathways. The control group received no treatment, while the HO group underwent treatment with 0.5 mM HO for a duration of 24 h. The tannic acid group received treatment with different concentrations of tannic acid for a duration of 24 h. Meanwhile, the tannic acid + HO group underwent pre-treatment with tannic acid for one hour and was subsequently subjected to 0.5 mM HO for one day. Within the tannic acid + HO group, the cell viability in SH-SY5Y cells was notably enhanced by tannic acid at concentrations of 2.5, 5, and 10 μM. It also resulted in a considerable rise in TAS (Total Antioxidant Status) levels and a concurrent decline in TOS (Total Oxidant Status) levels, serving as indicators of reduced oxidative stress. Additionally, tannic acid treatment resulted in decreased levels of apoptotic markers (Bax, cleaved PARP, and cleaved caspase 3) and oxidative DNA damage marker (8-oxo-dG), while increasing the anti-apoptotic marker Bcl-2. The findings from flow cytometry also revealed a significant reduction in the apoptosis rate following pretreatment with tannic acid. In summary, tannic acid demonstrates protective effects on SH-SY5Y cells in the face of HO-triggered oxidative damage by suppressing both oxidative stress and apoptosis. Nevertheless, additional research is warranted to assess the neuroprotective potential of tannic acid.
最近的研究表明，单宁酸与氧化损伤的减少有关。越来越多的证据支持单宁酸对中枢神经系统 (CNS) 的保护作用。然而，其对神经细胞中过氧化氢 (HO) 引发的氧化损伤的影响及其与细胞凋亡的相互作用仍存在不确定性。因此，本工作的目的是研究单宁酸对 HO 诱导氧化应激后 SH-SY5Y 细胞损伤的神经保护作用，特别是涉及细胞凋亡途径的作用。对照组未进行任何处理，HO 组用 0.5mM HO 处理 24 小时。单宁酸组用不同浓度的单宁酸处理 24 小时。同时，单宁酸+HO 组先用单宁酸预处理 1 小时，然后用 0.5mM HO 处理 1 天。在单宁酸+HO 组中，浓度为 2.5、5 和 10μM 的单宁酸可显著提高 SH-SY5Y 细胞的活力。它还导致 TAS（总抗氧化状态）水平显著升高，TOS（总氧化状态）水平显著降低，表明氧化应激减轻。此外，单宁酸处理降低了凋亡标志物（Bax、cleaved PARP 和 cleaved caspase 3）和氧化 DNA 损伤标志物（8-oxo-dG）的水平，同时增加了抗凋亡标志物 Bcl-2 的水平。流式细胞术的结果还显示，用单宁酸预处理后，细胞凋亡率显著降低。总之，单宁酸通过抑制氧化应激和细胞凋亡，对 HO 诱导的氧化损伤具有保护作用。然而，需要进一步研究来评估单宁酸的神经保护潜力。
