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

Wang SX, Wang J, Shao JB, Tang WN, Zhong JQ - Med. Sci. Monit. (2016)

Bottom Line: Inflammatory cytokine expressions were determined through ELISA.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Weifang People's Hospital, Weifang, Shandong, China (mainland).

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Plumbagin modulates NF-κB and Nrf-2 signaling pathway. NF-κB and Nrf-2 target proteins were determined by Western Blot. a. p<0.05, when compared to sham group. b. p<0.05, when compared to MI/R rats. Group I (sham); Group II (plumbagin); Group III (MI/R rats); Group III (plumbagin +MI/R). Results are given as the mean ±SEM for 10 rats in each group. (One-way ANOVA followed by Tukey’s multiple comparison).
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f3-medscimonit-22-1250: Plumbagin modulates NF-κB and Nrf-2 signaling pathway. NF-κB and Nrf-2 target proteins were determined by Western Blot. a. p<0.05, when compared to sham group. b. p<0.05, when compared to MI/R rats. Group I (sham); Group II (plumbagin); Group III (MI/R rats); Group III (plumbagin +MI/R). Results are given as the mean ±SEM for 10 rats in each group. (One-way ANOVA followed by Tukey’s multiple comparison).

Mentions: Myocardial I/R injury showed improved oxidative stress and inflammation by upregulation (p<0.05) of NF-κB and downregulation of Nrf-2 and their target gene expression compared to that of controls. Plumbagin treatment followed by MI/R injury induced Nrf-2 activation with concomitant increases (p<0.05) in HO-1, NQO1, and GST protein expression. Further, plumbagin reduced inflammatory markers such as NF-κB, COX-2, and iNOS protein expression (p<0.05) compared to that of MI/R injury rats (Figure 3).


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

Wang SX, Wang J, Shao JB, Tang WN, Zhong JQ - Med. Sci. Monit. (2016)

Plumbagin modulates NF-κB and Nrf-2 signaling pathway. NF-κB and Nrf-2 target proteins were determined by Western Blot. a. p<0.05, when compared to sham group. b. p<0.05, when compared to MI/R rats. Group I (sham); Group II (plumbagin); Group III (MI/R rats); Group III (plumbagin +MI/R). Results are given as the mean ±SEM for 10 rats in each group. (One-way ANOVA followed by Tukey’s multiple comparison).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4835155&req=5

f3-medscimonit-22-1250: Plumbagin modulates NF-κB and Nrf-2 signaling pathway. NF-κB and Nrf-2 target proteins were determined by Western Blot. a. p<0.05, when compared to sham group. b. p<0.05, when compared to MI/R rats. Group I (sham); Group II (plumbagin); Group III (MI/R rats); Group III (plumbagin +MI/R). Results are given as the mean ±SEM for 10 rats in each group. (One-way ANOVA followed by Tukey’s multiple comparison).
Mentions: Myocardial I/R injury showed improved oxidative stress and inflammation by upregulation (p<0.05) of NF-κB and downregulation of Nrf-2 and their target gene expression compared to that of controls. Plumbagin treatment followed by MI/R injury induced Nrf-2 activation with concomitant increases (p<0.05) in HO-1, NQO1, and GST protein expression. Further, plumbagin reduced inflammatory markers such as NF-κB, COX-2, and iNOS protein expression (p<0.05) compared to that of MI/R injury rats (Figure 3).

Bottom Line: Inflammatory cytokine expressions were determined through ELISA.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Weifang People's Hospital, Weifang, Shandong, China (mainland).

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus