Resveratrol attenuates 4-hydroxy-2-hexenal-induced oxidative stress in mouse cortical collecting duct cells.
10.4196/kjpp.2016.20.3.229
- Author:
Eun Hui BAE
1
;
Soo Yeon JOO
;
Seong Kwon MA
;
Jongun LEE
;
Soo Wan KIM
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju 61469, Korea. skimw@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
4-hydroxy-2-hexenal;
Collecting duct;
Oxidative stress;
Resveratrol;
Sirtuin 1
- MeSH:
Acetylcysteine;
Animals;
Anoxia;
Bays;
JNK Mitogen-Activated Protein Kinases;
Lipid Peroxidation;
Mice*;
Oxidative Stress*;
p38 Mitogen-Activated Protein Kinases;
Phosphotransferases;
Reactive Oxygen Species;
Sirtuin 1
- From:The Korean Journal of Physiology and Pharmacology
2016;20(3):229-236
- CountryRepublic of Korea
- Language:English
-
Abstract:
Resveratrol (RSV) may provide numerous protective eff ects against chronic inflammatory diseases. Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme oxidative stress, and aldehyde products formed during lipid peroxidation, such as 4-hydroxy-2-hexenal (HHE), might be responsible for tubular injury. This study aimed at investigating the eff ects of RSV on renal and its signaling mechanisms. While HHE treatment resulted in decreased expression of Sirt1, AQP2, and nuclear factor erythroid 2-related factor 2 (Nrf2), mouse cortical collecting duct cells (M1) cells treated with HHE exhibited increased activation of p38 MAPK, extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and increased expression of NOX4, p47(phox), Kelch ECH associating protein 1 (Keap1) and COX2. HHE treatment also induced NF-κB activation by promoting IκB-α degradation. Meanwhile, the observed increases in nuclear NF-κB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV. Our findings indicate that RSV inhibits the expression of inflammatory proteins and the production of reactive oxygen species in M1 cells by inhibiting NF-κB activation.
