Resveratrol improves intestinal barrier function, alleviates mitochondrial dysfunction and induces mitophagy in diquat challenged piglets1
Resveratrol improves intestinal barrier function, alleviates mitochondrial dysfunction and induces mitophagy in diquat challenged piglets1
复制标题
白藜芦醇改善敌草快挑战仔猪的肠道屏障功能，减轻线粒体功能障碍并诱导线粒体自噬1
DOI：
10.1039/c8fo02091d
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发表时间：
2019-01-01
期刊：
影响因子：
6.1
通讯作者：
Hu, Caihong
中科院分区：
文献类型：
--
作者：
Cao, Shuting;Shen, Zhuojun;Hu, Caihong
本研究旨在探讨白藜芦醇是否能减轻敌草快诱导的仔猪氧化应激引起的肠道损伤，增强线粒体功能和线粒体自噬水平。将24头35日龄仔猪随机分为4组：（1）对照组;（2）对照组+ 100 mg kg-1白藜芦醇组;（3）敌草快对照组;（4）敌草快+ 100 mg kg-1白藜芦醇组。在实验开始时，给仔猪注射敌草快或生理盐水（10 mg/kg体重）。在第14天，处死仔猪以获得空肠段。结果表明，与敌草快组相比，白藜芦醇组空肠黏膜总抗氧化能力（T-AOC）显著提高（P <0.05），过氧化氢（H2 O2）和丙二醛（MDA）水平显著降低（P <0.05）。白藜芦醇能显著改善肠黏膜屏障功能（P < 0.05），表现为空肠黏膜上皮细胞跨膜电阻增加和细胞外膜荧光素异硫氰酸酯葡聚糖4kDa通透性降低。此外，白藜芦醇还能显著抑制敌草快引起的空肠黏膜occludin、claudin-1和ZO-1水平的下降（P < 0.05）。白藜芦醇能改善敌草快诱导的线粒体肿胀、空泡化和嵴断裂。白藜芦醇能显著降低空肠线粒体活性氧的产生（P <0.05），提高空肠线粒体膜电位、线粒体DNA含量和线粒体复合物Ⅰ-Ⅳ的活性（P < 0.05）。白藜芦醇可显著提高肠线粒体中PINK 1和Parkin的表达水平（P < 0.05），同时增加空肠中LC 3-II/LC 3-I的比值（P < 0.05）。这些数据表明，白藜芦醇是有效的保护肠道屏障，改善氧化还原状态，减轻线粒体损伤和诱导线粒体自噬在敌草快攻击仔猪。
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.