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10.12659/MSM.897618

http://scihub22266oqcxt.onion/10.12659/MSM.897618
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C4835155!4835155!27078001
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suck abstract from ncbi


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pmid27078001      Med+Sci+Monit 2016 ; 22 (ä): 1250-7
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  • Plumbagin Mediates Cardioprotection Against Myocardial Ischemia/Reperfusion Injury Through Nrf-2 Signaling #MMPMID27078001
  • Wang SX; Wang J; Shao JB; Tang Wn; Zhong JQ
  • Med Sci Monit 2016[]; 22 (ä): 1250-7 PMID27078001show ga
  • 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/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-?B and Nrf-2. Further, downstream targets of NF-?B (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.
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