4.3 Article

Toxicity assessment of hydrogen peroxide on Toll-like receptor system, apoptosis, and mitochondrial respiration in piglets and IPEC-J2 cells

期刊

ONCOTARGET
卷 8, 期 2, 页码 3124-3131

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.13844

关键词

H2O2; TLRs; apoptosis; mitochondrial respiration; piglet

资金

  1. National Basic Research Program of China [2013CB127301]
  2. National Key RD Program [2016YFD0501201]
  3. Key Programs of frontier scientific research of the Chinese Academy of Sciences [QYZDY-SSW-SMC008]
  4. National Natural Science Foundation of China [31272463]
  5. Changsha City Science and Technology Program of China [k1508008-21]
  6. Hunan Province Key project [2015NK1002]
  7. Hunan Provincial Natural Science Foundation of China [12JJ2014]

向作者/读者索取更多资源

In this study, expressions of toll-like receptors (TLRs) and apoptosis-related genes in piglets and mitochondrial respiration in intestinal porcine epithelial cells were investigated after hydrogen peroxide (H2O2) exposure. The in vivo results showed that H2O2 influenced intestinal expressions of TLRs and apoptosis related genes. H2O2 treatment (5% and 10%) downregulated uncoupling protein 2 (UCP2) expression in the duodenum (P < 0.05), while low dosage of H2O2 significantly increased UCP2 expression in the jejunum (P < 0.05). In IPEC-J2 cells, H2O2 inhibited cell proliferation (P < 0.05) and caused mitochondrial dysfunction via reducing maximal respiration, spare respiratory, non-mitochondrial respiratory, and ATP production (P < 0.05). However, 50 uM H2O2 significantly enhanced mitochondrial proton leak (P < 0.05). In conclusion, H2O2 affected intestinal TLRs system, apoptosis related genes, and mitochondrial dysfunction in vivo and in vitro models. Meanwhile, low dosage of H2O2 might exhibit a feedback regulatory mechanism against oxidative injury via increasing UCP2 expression and mitochondrial proton leak.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.3
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据