白藜芦醇通过 Nrf2 信号通路对脱氧雪腐镰刀菌烯醇诱导的猪肠上皮细胞损伤的保护作用。
Protection of Porcine Intestinal-Epithelial Cells from Deoxynivalenol-Induced Damage by Resveratrol via the Nrf2 Signaling Pathway.
机构信息
College of Animal Science , South China Agricultural University , Guangzhou 510642 , PR China.
Agro-biological Gene Research Center , Guangdong Academy of Agricultural Sciences , Guangzhou 510640 , PR China.
出版信息
J Agric Food Chem. 2019 Feb 13;67(6):1726-1735. doi: 10.1021/acs.jafc.8b03662. Epub 2019 Feb 4.
Deoxynivalenol (DON), a common mycotoxin, usually induces oxidative stress and affects the intestinal health of humans and animals. This study investigated the protective effect of resveratrol (RES), a natural antioxidant, on alleviating the cytotoxicity induced by DON in the porcine intestinal-epithelial cell line (IPEC-J2). Cells were incubated with RES for 24 h and then exposed to DON for another 24 h. Cell viability, proliferation, apoptosis, and oxidative-stress indicators were determined. In comparison with DON-only-treated cells, pretreatment with RES (15 μM) increased the cell viability (79.74 ± 2.02 vs 90.98 ± 2.66%, P < 0.01), improved proliferation (EdU-positive cells, 26.42 ± 1.12 vs 32.05 ± 0.78%, P < 0.01), decreased accumulation of intracellular reactive oxygen species (ROS, 1.68 ± 0.05 vs 1.29 ± 0.06, P < 0.01), stabilized mitochondrial-membrane potential (MMP, 8.98 ± 1.40 vs 2.29 ± 0.76, P < 0.001), and prevented apoptosis induced by DON (13.91 ± 1.20 vs 6.83 ± 0.52%, P < 0.01). RES activated the Nrf2 signaling pathway, and transfection with Nrf2 siRNA abrogated the protection of RES against DON-induced cytotoxicity, accumulation of intracellular ROS, and mitochondria-dependent apoptosis. Collectively, RES protects IPEC-J2 cells against DON-induced damage at least partly via the Nrf2 signaling pathway.
脱氧雪腐镰刀菌烯醇（DON）是一种常见的霉菌毒素，通常会诱导氧化应激，影响人类和动物的肠道健康。本研究探讨了白藜芦醇（RES），一种天然抗氧化剂，对缓解猪肠上皮细胞系（IPEC-J2）中 DON 诱导的细胞毒性的保护作用。将细胞用 RES 孵育 24 小时，然后再暴露于 DON 24 小时。测定细胞活力、增殖、凋亡和氧化应激指标。与仅用 DON 处理的细胞相比，用 RES（15 μM）预处理增加了细胞活力（79.74 ± 2.02%比 90.98 ± 2.66%，P < 0.01），改善了增殖（EdU 阳性细胞，26.42 ± 1.12%比 32.05 ± 0.78%，P < 0.01），减少了细胞内活性氧（ROS）的积累（1.68 ± 0.05%比 1.29 ± 0.06%，P < 0.01），稳定了线粒体膜电位（MMP，8.98 ± 1.40%比 2.29 ± 0.76%，P < 0.001），并阻止了 DON 诱导的凋亡（13.91 ± 1.20%比 6.83 ± 0.52%，P < 0.01）。RES 激活了 Nrf2 信号通路，而用 Nrf2 siRNA 转染则消除了 RES 对 DON 诱导的细胞毒性、细胞内 ROS 积累和线粒体依赖性凋亡的保护作用。综上所述，RES 通过 Nrf2 信号通路至少部分保护 IPEC-J2 细胞免受 DON 诱导的损伤。
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