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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 reduces oxidative stress in rats with cardiac I/R injury. (A) Plumbagin inhibits ROS generation: The results are expressed as ROS generated (%) when compared to sham rats. (B) Plumbagin inhibits Lipid peroxidation: The results are expressed as nanomoles of TBARS formed/mg of protein. Results are expressed in nM/mg of protein. a. p<0.05, when compared to sham group. b. p<0.05, when compared to I/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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f1-medscimonit-22-1250: Plumbagin reduces oxidative stress in rats with cardiac I/R injury. (A) Plumbagin inhibits ROS generation: The results are expressed as ROS generated (%) when compared to sham rats. (B) Plumbagin inhibits Lipid peroxidation: The results are expressed as nanomoles of TBARS formed/mg of protein. Results are expressed in nM/mg of protein. a. p<0.05, when compared to sham group. b. p<0.05, when compared to I/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: Reactive oxygen species generation and lipid peroxide content was significantly higher (p<0.05) during myocardial I/R injury in Wistar rats compared to control. Plumbagin treatment reduced the oxidative stress by decreasing ROS and lipid peroxide content (p<0.05) compared to myocardial I/R injury rats (Figure 1).


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 reduces oxidative stress in rats with cardiac I/R injury. (A) Plumbagin inhibits ROS generation: The results are expressed as ROS generated (%) when compared to sham rats. (B) Plumbagin inhibits Lipid peroxidation: The results are expressed as nanomoles of TBARS formed/mg of protein. Results are expressed in nM/mg of protein. a. p<0.05, when compared to sham group. b. p<0.05, when compared to I/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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f1-medscimonit-22-1250: Plumbagin reduces oxidative stress in rats with cardiac I/R injury. (A) Plumbagin inhibits ROS generation: The results are expressed as ROS generated (%) when compared to sham rats. (B) Plumbagin inhibits Lipid peroxidation: The results are expressed as nanomoles of TBARS formed/mg of protein. Results are expressed in nM/mg of protein. a. p<0.05, when compared to sham group. b. p<0.05, when compared to I/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: Reactive oxygen species generation and lipid peroxide content was significantly higher (p<0.05) during myocardial I/R injury in Wistar rats compared to control. Plumbagin treatment reduced the oxidative stress by decreasing ROS and lipid peroxide content (p<0.05) compared to myocardial I/R injury rats (Figure 1).

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