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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 enhances antioxidant status. Antioxidant enzyme activities -SOD, CAT, GST, and GPx are expressed in units/mg protein. GSH is expressed as nmol of GSH/mg of protein. Results are given as the mean ±SEM for 10 rats in each group. 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). (One-way ANOVA followed by Tukey’s multiple comparison).
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f2-medscimonit-22-1250: Plumbagin enhances antioxidant status. Antioxidant enzyme activities -SOD, CAT, GST, and GPx are expressed in units/mg protein. GSH is expressed as nmol of GSH/mg of protein. Results are given as the mean ±SEM for 10 rats in each group. 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). (One-way ANOVA followed by Tukey’s multiple comparison).

Mentions: Myocardial I/R injury was significantly less (p<0.05) in the enzymic and non-enzymic antioxidant defense system of GSH, SOD, CAT, GPX, and GST activities compared to that of sham rats. Rats treated with plumbagin followed by MI/R injury had better (p<0.05) antioxidant status than myocardial I/R injury rats (Figure 2).


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 enhances antioxidant status. Antioxidant enzyme activities -SOD, CAT, GST, and GPx are expressed in units/mg protein. GSH is expressed as nmol of GSH/mg of protein. Results are given as the mean ±SEM for 10 rats in each group. 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). (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

f2-medscimonit-22-1250: Plumbagin enhances antioxidant status. Antioxidant enzyme activities -SOD, CAT, GST, and GPx are expressed in units/mg protein. GSH is expressed as nmol of GSH/mg of protein. Results are given as the mean ±SEM for 10 rats in each group. 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). (One-way ANOVA followed by Tukey’s multiple comparison).
Mentions: Myocardial I/R injury was significantly less (p<0.05) in the enzymic and non-enzymic antioxidant defense system of GSH, SOD, CAT, GPX, and GST activities compared to that of sham rats. Rats treated with plumbagin followed by MI/R injury had better (p<0.05) antioxidant status than myocardial I/R injury rats (Figure 2).

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