Plumbagin Mediates Cardioprotection Against Myocardial Ischemia/Reperfusion Injury Through Nrf-2 Signaling

BACKGROUND Plumbagin is a potent antioxidant with anti-inflammatory and anti-carcinogenic action. Myocardial ischemia/reperfusion injury results in organ damage through oxidative stress and inflammatory mechanisms. In this study, we analyzed the potential role of plumbagin against myocardial I/R inj...

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Bibliographic Details
Published in:Medical science monitor 2016-04, Vol.22, p.1250-1257
Main Authors: Wang, Shi-Xun, Wang, Jian, Shao, Jing-Bo, Tang, Wei-Ning, Zhong, Jing-Quan
Format: Article
Language:English
Subjects:
Animal Study
Animals
Anti-Inflammatory Agents - pharmacology
Anticarcinogenic Agents - pharmacology
Antioxidants - pharmacology
Apoptosis - drug effects
Lipid Peroxidation - drug effects
Male
Mice
Mice, Inbred C57BL
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - prevention & control
Naphthoquinones - pharmacology
NF-E2-Related Factor 2 - metabolism
NF-kappa B - metabolism
Oxidative Stress - drug effects
Random Allocation
Rats
Rats, Wistar
Signal Transduction - drug effects
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Summary:BACKGROUND Plumbagin is a potent antioxidant with anti-inflammatory and anti-carcinogenic action. Myocardial ischemia/reperfusion injury results in organ damage through oxidative stress and inflammatory mechanisms. In this study, we analyzed the potential role of plumbagin against myocardial I/R injury in Wistar rats. MATERIAL AND METHODS Oxidative stress was measured through ROS, lipid peroxide content, and antioxidant enzyme activities. The expression of redox signaling and inflammatory proteins was analyzed through Western blotting. Inflammatory cytokine expressions were determined through ELISA. RESULTS Oxidative stress status was reduced by plumbagin by decreasing ROS and lipid peroxide levels in rats with myocardial I/R (MI/R) injury. Plumbagin regulated redox imbalance induced by I/R injury by modulating the transcription factors NF-κB and Nrf-2. Further, downstream targets of NF-κB (COX-2, iNOS) and Nrf-2 (HO-1, NQO1 and GST) expression were significantly downregulated by plumbagin treatment. Pro-inflammatory cytokine expressions were significantly abrogated by plumbagin treatment. CONCLUSIONS This study shows the protective role of plumbagin against myocardial I/R injury by regulating antioxidant and inflammatory mechanisms.
ISSN:1643-3750
1234-1010
1643-3750
DOI:10.12659/MSM.897618