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.

Keywords: Anti-Inflammatory Agents - pharmacology, Anticarcinogenic Agents - pharmacology, Antioxidants - pharmacology, Lipid Peroxidation - drug effects, Myocardial Reperfusion Injury - prevention & control, NF-E2-Related Factor 2 - metabolism, Naphthoquinones - pharmacology, Oxidative Stress - drug effects, Random Allocation, Signal Transduction - drug effects