Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction

González-Salazar, Alfredo; Molina‐Jijón, Eduardo; Correa, Francisco; Zarco-Márquez, Guillermo; Calderón‐Oliver, Mariel; Tapia, Edilia; Zazueta, Cecilia; Pedraza‐Chaverrí, José

doi:10.1007/s12012-011-9128-9

Cited by 73 publications

(60 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The depletion of mitochondrial GSH and NP-SH has been shown to be associated with xenobiotic-induced toxicity (González-Salazar et al 2011). The level of GSH and NP-SH, which were affected by Oxa treatment, was also strengthened toward normal level by CMN and QR pretreatment.…”

Section: Discussionmentioning

confidence: 97%

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

View full text Add to dashboard Cite

Peripheral neurotoxicity is one of the serious dose-limiting side effects of oxaliplatin (Oxa) when used in the treatment of malignant conditions. It is documented that it elicits major side effects specifically neurotoxicity due to oxidative stress forcing the patients to limit its clinical use in long-term treatment. Oxidative stress has been proven to be involved in Oxa-induced toxicity including neurotoxicity. The mitochondria have recently emerged as targets for anticancer drugs in various kinds of toxicity including neurotoxicity that can lead to neoplastic disease. However, there is paucity of literature involving the role of the mitochondria in mediating Oxa-induced neurotoxicity and its underlying mechanism is still debatable. The purpose of this study was to investigate the dose-dependent damage caused by Oxa on isolated brain mitochondria under in vitro conditions. The study was also designed to investigate the neuroprotective effects of nutraceuticals, curcumin (CMN), and quercetin (QR) on Oxa-induced mitochondrial oxidative stress and respiratory chain complexes in the brain of rats. Oxidative stress biomarkers, levels of nonenzymatic antioxidants, activities of enzymatic antioxidants, and mitochondrial complexes were evaluated against the neurotoxicity induced by Oxa. Pretreatment with CMN and QR significantly replenished the mitochondrial lipid peroxidation levels and protein carbonyl content induced by Oxa. CMN and QR ameliorated altered nonenzymatic and enzymatic antioxidants and complex enzymes of mitochondria. We conclude that CMN and QR, by attenuating oxidative stress as evident by mitochondrial dysfunction, hold promise as agents that can potentially reduce Oxa-induced adverse effects in the brain.

show abstract

Section: Discussionmentioning

confidence: 97%

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

View full text Add to dashboard Cite

show abstract

“…The principal functions of curcumin include: i) Anti-inflammation: Curcumin functions in alleviating the pain induced by inflammation predominantly by activating inflammatory mediators such as lipoxygenase and cyclooxygenase, and transcription factors such as activator protein-1 (14,15); ii) antioxidant: There are two benzene rings in the chemical structure of curcumin, with one ring having a phenol hydroxy and the other a phenol methoxy. These are able to eliminate oxygen free radicals, serve as hydrogen donors or adjust other mediators involved in the oxidation reaction against antioxidant and anti-lipid peroxidation; iii) regulation of blood lipids: Curcumin may lower the level of total cholesterol, triglyceride and low density lipoprotein, increase the level of high-density lipoprotein, inhibit the oxidative modification of low density lipoprotein (16), and reduce the damage to the vessel walls by oxidized low density lipoprotein; iv) curcumin may also reduce myocardial ischemia re-perfusion injury (17), lower blood viscosity, inhibit the formation of atherosclerotic plaque, stabilize plaque and inhibit adaptive hypertrophy (18,19) of the myocardium following myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-κB, PPAR-γ and Bcl-2 in rats with myocardial infarction injury

Yin

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Curcumin is a natural polyphenol with powerful antioxidant and anti-inflammatory properties. The present study evaluated the protective effect of curcumin on myocardial injury in rats as well as the mechanisms underlying these effects, and examined the expression of nuclear factor-κB (NF-κB), peroxisome proliferator-activated receptor-γ (PPAR-γ) and B-cell leukemia/lymphoma-2 (Bcl-2) following myocardial infarction. A rat model of myocardial infarction was successfully established. Hematoxylin and eosin staining showed cellular atrophy and hyperchromatic cytoplasm in the myocardial infarction area. The myocardial cells displayed lysis and breakage of cardiac muscle fibers, karyopyknosis and karyorrhexis associated with infiltration of inflammatory cells and proliferation of fibrous tissue. Curcumin treatment at a dosage of 150 mg/kg/body weight resulted in an increase in surviving cells, fewer apoptotic cells, decreased proliferation of fibrous tissue and reduced infiltration of inflammatory cells, though necrosis was still present compared with the rats without curcumin treatment. The immunohistochemical assay demonstrated that curcumin treatment inhibited the expression of NF-κB, but increased the expression of PPAR-γ. The results of the reverse transcription-polymerase chain reaction indicated that curcumin treatment significantly increased the mRNA expression levels of Bcl-2 (P<0.01). Therefore, curcumin antagonizes cardiomyocyte apoptosis and inhibits inflammatory cell infiltration following myocardial infarction, which may be associated with its inhibitory effects on the expression of NF-κB, and activating effects on the expression of PPAR-γ and Bcl-2 in myocardial cells. Curcumin may be useful in clinical practice for saving more living heart muscle in the area of myocardial infarction and improving cardiac function following the elective opening of obstructed coronary arteries.

show abstract

“…9) Lastly, the protective effects of curcumin on oxidative injury have been demonstrated in vivo in several animal diseases models. [10][11][12] Free radicals are normally formed by the physiological processes of the cell. For example superoxide anion radical (O 2 −· ) is produced during the mitochondrial respiratory chain reaction and the nitric oxide radical (NO) is generated by the activation of nitric oxide synthase.…”

mentioning

confidence: 99%

Electron Paramagnetic Resonance Study of the Free Radical Scavenging Capacity of Curcumin and Its Demethoxy and Hydrogenated Derivatives

Morales

Sirijaroonwong

Yamanont

et al. 2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The quantitative free radical scavenging capacity of curcumin and its demethoxy derivatives (demethoxycurcumin (Dmc) and bisdemethoxycurcumin (Bdmc)) and hydrogenated derivatives (tetrahydrocurcumin (THC), hexahydrocurcumin (HHC) and octahydrocurcumin (OHC)) towards 1,1-diphenyl-2-picryl hydrazyl (DPPH), nitric oxide radical (NO), hydroxyl radical (HO · ) and superoxide anion radical (O 2 · ) were investigated by electron paramagnetic resonance (EPR) spectroscopy. One mole of the hydrogenated derivatives scavenged about 4 mol of the DPPH radical, while curcumin and Dmc scavenged about 3 mol of the DPPH radical. Curcumin and THC showed moderate scavenging activity towards NO, yielding 200 mmol of NO scavenged per 1 mol of the scavenger. In contrast, curcumin and its derivatives showed very low scavenging activity towards HO · and O 2 · , yielding approximately only 3-12 mmol scavenged per 1 mol of the tested compounds. Our results suggest that curcumin and its derivatives principally act as chain breaking antioxidants rather than as direct free radical scavengers. Furthermore, we showed that the ortho-methoxyphenolic group and the heptadione linkage of these molecules greatly contributed to their DPPH and NO scavenging activity.Key words curcumin; electron paramagnetic resonance; free radical scavenger; spin trapping Curcumin [1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] is the primary biologically active constituent that is isolated from the spice, turmeric (Curcuma longa LINN). It shows various therapeutically beneficial activities, including anti-oxidant, anti-inflammatory, anti-cancer, and anti-viral activities 1,2) mediated through its interactions with several molecular targets such as enzymes, receptors, and transcription factors.3,4) As a potent anti-oxidant, several mechanisms have been proposed which describe the direct interaction of curcumin with reactive oxygen species (ROS) as well as its involvement in ROS-independent mechanisms (i.e., induction of antioxidant enzymes). 5,6) The structure-antioxidant activity relationship of curcumin and the compound it reduces has been demonstrated in both in vitro and in vivo models, for example, 1,1-diphenyl-2-picrylhydrazyl (DPPH) kinetic analysis, γ-radiolysis of rat liver microsomes, 7) 2,2′-azobis(2-amidinopropane)dihydrochloride (AAPH)-induced low density lipoprotein (LDL) oxidation, 8) AAPH-induced linoleic oxidation. 9) Lastly, the protective effects of curcumin on oxidative injury have been demonstrated in vivo in several animal diseases models. [10][11][12] Free radicals are normally formed by the physiological processes of the cell. For example superoxide anion radical (O 2 −· ) is produced during the mitochondrial respiratory chain reaction and the nitric oxide radical (NO) is generated by the activation of nitric oxide synthase. In some circumstances, the overproduction of those radicals, as well as the formation of toxic radicals such as the hydroxyl radical (HO · ) leads to the damage of biological molecules, thus resulting in many ...

show abstract

Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction

Cited by 73 publications

References 37 publications

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-κB, PPAR-γ and Bcl-2 in rats with myocardial infarction injury

Electron Paramagnetic Resonance Study of the Free Radical Scavenging Capacity of Curcumin and Its Demethoxy and Hydrogenated Derivatives

Contact Info

Product

Resources

About