Animal Science College, Zhejiang University, Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, Hangzhou, 310058, China.
Food Funct. 2019 Jan 22;10(1):344-354. doi: 10.1039/c8fo02091d.
This study evaluated whether resveratrol can alleviate intestinal injury and enhance the mitochondrial function and the mitophagy level in diquat induced oxidative stress of piglets. Twenty-four 35 day old piglets were randomly allocated to four groups: (1) nonchallenged control; (2) control + 100 mg kg-1 resveratrol diet; (3) diquat-treated control and (4) diquat + 100 mg kg-1 resveratrol diet. At the beginning of the experiment, the piglets were injected with diquat or saline (10 mg per kg bodyweight). On day 14, the piglets were killed to obtain the jejuna segments. The results showed that resveratrol increased (P < 0.05) the total antioxidant capacity (T-AOC) and decreased (P < 0.05) the hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in the jejunal mucosa, in comparison with the diquat group. Resveratrol improved (P < 0.05) the intestinal barrier function, as indicated by the increased transepithelial electrical resistance and the decreased paracellular permeability of fluorescein isothiocyanate dextran 4 kDa in the jejunum. Moreover, resveratrol prevented (P < 0.05) the diquat induced decline of occludin, claudin-1 and ZO-1 levels in the jejunal mucosa. Resveratrol ameliorated mitochondria swelling, vacuolation and cracked cristae induced by diquat. Resveratrol decreased (P < 0.05) the ROS generation and increased (P < 0.05) the membrane potential of intestinal mitochondria, the content of mitochondrial DNA and the activity of mitochondrial complexes I-IV in the jejunum. Finally, resveratrol enhanced (P < 0.05) the level of PTEN induced putative kinase 1 (PINK1) and Parkin in intestinal mitochondria; meanwhile it increased (P < 0.05) the LC3-II/LC3-I ratio in the jejunum. These data indicate that resveratrol is effective in protecting the intestinal barrier, improving the redox status, alleviating mitochondrial damage and inducing mitophagy in piglets challenged with diquat.
本研究旨在评估白藜芦醇是否可以减轻二氯二氢对猪的氧化应激诱导的肠道损伤，并增强线粒体功能和自噬水平。将 24 头 35 日龄仔猪随机分为 4 组：（1）未应激对照；（2）对照+100mgkg-1白藜芦醇饮食；（3）二氯二氢处理对照和（4）二氯二氢+100mgkg-1白藜芦醇饮食。在实验开始时，仔猪注射二氯二氢或生理盐水（每公斤体重 10mg）。第 14 天，处死仔猪以获得空肠段。结果显示，与二氯二氢组相比，白藜芦醇增加（P<0.05）空肠黏膜的总抗氧化能力（T-AOC），降低（P<0.05）过氧化氢（H2O2）和丙二醛（MDA）水平。白藜芦醇改善（P<0.05）肠道屏障功能，表现为空肠上皮细胞间电阻增加，荧光素异硫氰酸酯葡聚糖 4kDa 的旁通透性降低。此外，白藜芦醇防止（P<0.05）二氯二氢诱导的空肠黏膜occludin、claudin-1 和 ZO-1 水平下降。白藜芦醇改善了二氯二氢引起的线粒体肿胀、空泡化和嵴破裂。白藜芦醇降低（P<0.05）ROS 的产生，增加（P<0.05）空肠线粒体的膜电位、线粒体 DNA 含量和线粒体复合物 I-IV 的活性。最后，白藜芦醇增强（P<0.05）肠线粒体中 PTEN 诱导的假定激酶 1（PINK1）和 Parkin 的水平；同时，它增加（P<0.05）空肠中 LC3-II/LC3-I 比值。这些数据表明，白藜芦醇在保护仔猪肠道屏障、改善氧化还原状态、减轻线粒体损伤和诱导自噬方面是有效的。
