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Renoprotective effect of the antioxidant curcumin: Recent findings.

Trujillo J, Chirino YI, Molina-Jijón E, Andérica-Romero AC, Tapia E, Pedraza-Chaverrí J - Redox Biol (2013)

Bottom Line: Another recent finding shows that the renoprotective effect of curcumin is associated to preservation of function and redox balance of mitochondria.Taking together, these studies attribute the protective effect of curcumin in the kidney to the induction of the master regulator of antioxidant response nuclear factor erythroid-derived 2 (Nrf2), inhibition of mitochondrial dysfunction, attenuation of inflammatory response, preservation of antioxidant enzymes and prevention of oxidative stress.The information presented in this paper identifies curcumin as a promising renoprotective molecule against renal injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Facultad de Química, UNAM, Ciudad Universitaria, 04510 México, DF, Mexico.

ABSTRACT
For years, there have been studies based on the use of natural compounds plant-derived as potential therapeutic agents for various diseases in humans. Curcumin is a phenolic compound extracted from Curcuma longa rhizome commonly used in Asia as a spice, pigment and additive. In traditional medicine of India and China, curcumin is considered as a therapeutic agent used in several foods. Numerous studies have shown that curcumin has broad biological functions particularly antioxidant and antiinflammatory. In fact, it has been established that curcumin is a bifunctional antioxidant; it exerts antioxidant activity in a direct and an indirect way by scavenging reactive oxygen species and inducing an antioxidant response, respectively. The renoprotective effect of curcumin has been evaluated in several experimental models including diabetic nephropathy, chronic renal failure, ischemia and reperfusion and nephrotoxicity induced by compounds such as gentamicin, adriamycin, chloroquine, iron nitrilotriacetate, sodium fluoride, hexavalent chromium and cisplatin. It has been shown recently in a model of chronic renal failure that curcumin exerts a therapeutic effect; in fact it reverts not only systemic alterations but also glomerular hemodynamic changes. Another recent finding shows that the renoprotective effect of curcumin is associated to preservation of function and redox balance of mitochondria. Taking together, these studies attribute the protective effect of curcumin in the kidney to the induction of the master regulator of antioxidant response nuclear factor erythroid-derived 2 (Nrf2), inhibition of mitochondrial dysfunction, attenuation of inflammatory response, preservation of antioxidant enzymes and prevention of oxidative stress. The information presented in this paper identifies curcumin as a promising renoprotective molecule against renal injury.

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Curcumin is able to prevent mitochondrial dysfunction associated to renal injury. Curcumin is able to prevent lipid peroxidation and the decrease in the following mitochondrial determinations: oxygen consumption, activity of complexes I, II, II-III and V, activity of aconitase and antioxidant enzymes, GSH content, membrane potential, calcium retention and ATP content [51]. GSH (Glutathione), SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), GST (glutathione-S-transferase), GR (glutathione reductase), NAD+ (nicotinamide adenine dinucleotide), NADH (nicotinamide adenine dinucleotide, reduced form), FAD+ (flavin adenine dinucleotide), FADH2 (flavin adenine dinucleotide, reduced form), ATP (adenosine triphosphate), ADP (adenosine diphosphate).
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f0015: Curcumin is able to prevent mitochondrial dysfunction associated to renal injury. Curcumin is able to prevent lipid peroxidation and the decrease in the following mitochondrial determinations: oxygen consumption, activity of complexes I, II, II-III and V, activity of aconitase and antioxidant enzymes, GSH content, membrane potential, calcium retention and ATP content [51]. GSH (Glutathione), SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), GST (glutathione-S-transferase), GR (glutathione reductase), NAD+ (nicotinamide adenine dinucleotide), NADH (nicotinamide adenine dinucleotide, reduced form), FAD+ (flavin adenine dinucleotide), FADH2 (flavin adenine dinucleotide, reduced form), ATP (adenosine triphosphate), ADP (adenosine diphosphate).

Mentions: Studies evaluating the effect of curcumin in experimental models of nephrotoxicity by heavy metals such as chromium (Cr) [51], cadmium [30] and mercury (Hg) [1] have been conducted. Curcumin treatment attenuated renal dysfunction, oxidative stress and the decrease in antioxidant enzymes induced by metals. Interestingly, Molina-Jijón et al. [51] demonstrated that curcumin has a protective effect against nephrotoxicity induced by hexavalent chromium (Cr VI), and this property was related to the nuclear translocation of Nrf2, prevention of oxidant stress and preservation of the activity of antioxidant enzymes and of mitochondrial function in the kidney. In this study, a pretreatment of 10-day with 400 mg/kg of curcumin attenuated the structural and functional damage to the kidney which was associated with the prevention of mitochondrial oxidant stress and of the decrease in the following mitochondrial determinations: oxygen consumption (state 3), respiratory control, ATP content, calcium retention and membrane potential. Also curcumin prevented the decrease in the following enzymatic activities: aconitase, antioxidant enzymes and mitochondrial respiratory complexes I, II, II–III and V [51], (Fig. 3). This was the first demonstration that the prevention of renal injury was associated to the preservation of mitochondrial function.


Renoprotective effect of the antioxidant curcumin: Recent findings.

Trujillo J, Chirino YI, Molina-Jijón E, Andérica-Romero AC, Tapia E, Pedraza-Chaverrí J - Redox Biol (2013)

Curcumin is able to prevent mitochondrial dysfunction associated to renal injury. Curcumin is able to prevent lipid peroxidation and the decrease in the following mitochondrial determinations: oxygen consumption, activity of complexes I, II, II-III and V, activity of aconitase and antioxidant enzymes, GSH content, membrane potential, calcium retention and ATP content [51]. GSH (Glutathione), SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), GST (glutathione-S-transferase), GR (glutathione reductase), NAD+ (nicotinamide adenine dinucleotide), NADH (nicotinamide adenine dinucleotide, reduced form), FAD+ (flavin adenine dinucleotide), FADH2 (flavin adenine dinucleotide, reduced form), ATP (adenosine triphosphate), ADP (adenosine diphosphate).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3814973&req=5

f0015: Curcumin is able to prevent mitochondrial dysfunction associated to renal injury. Curcumin is able to prevent lipid peroxidation and the decrease in the following mitochondrial determinations: oxygen consumption, activity of complexes I, II, II-III and V, activity of aconitase and antioxidant enzymes, GSH content, membrane potential, calcium retention and ATP content [51]. GSH (Glutathione), SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), GST (glutathione-S-transferase), GR (glutathione reductase), NAD+ (nicotinamide adenine dinucleotide), NADH (nicotinamide adenine dinucleotide, reduced form), FAD+ (flavin adenine dinucleotide), FADH2 (flavin adenine dinucleotide, reduced form), ATP (adenosine triphosphate), ADP (adenosine diphosphate).
Mentions: Studies evaluating the effect of curcumin in experimental models of nephrotoxicity by heavy metals such as chromium (Cr) [51], cadmium [30] and mercury (Hg) [1] have been conducted. Curcumin treatment attenuated renal dysfunction, oxidative stress and the decrease in antioxidant enzymes induced by metals. Interestingly, Molina-Jijón et al. [51] demonstrated that curcumin has a protective effect against nephrotoxicity induced by hexavalent chromium (Cr VI), and this property was related to the nuclear translocation of Nrf2, prevention of oxidant stress and preservation of the activity of antioxidant enzymes and of mitochondrial function in the kidney. In this study, a pretreatment of 10-day with 400 mg/kg of curcumin attenuated the structural and functional damage to the kidney which was associated with the prevention of mitochondrial oxidant stress and of the decrease in the following mitochondrial determinations: oxygen consumption (state 3), respiratory control, ATP content, calcium retention and membrane potential. Also curcumin prevented the decrease in the following enzymatic activities: aconitase, antioxidant enzymes and mitochondrial respiratory complexes I, II, II–III and V [51], (Fig. 3). This was the first demonstration that the prevention of renal injury was associated to the preservation of mitochondrial function.

Bottom Line: Another recent finding shows that the renoprotective effect of curcumin is associated to preservation of function and redox balance of mitochondria.Taking together, these studies attribute the protective effect of curcumin in the kidney to the induction of the master regulator of antioxidant response nuclear factor erythroid-derived 2 (Nrf2), inhibition of mitochondrial dysfunction, attenuation of inflammatory response, preservation of antioxidant enzymes and prevention of oxidative stress.The information presented in this paper identifies curcumin as a promising renoprotective molecule against renal injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Facultad de Química, UNAM, Ciudad Universitaria, 04510 México, DF, Mexico.

ABSTRACT
For years, there have been studies based on the use of natural compounds plant-derived as potential therapeutic agents for various diseases in humans. Curcumin is a phenolic compound extracted from Curcuma longa rhizome commonly used in Asia as a spice, pigment and additive. In traditional medicine of India and China, curcumin is considered as a therapeutic agent used in several foods. Numerous studies have shown that curcumin has broad biological functions particularly antioxidant and antiinflammatory. In fact, it has been established that curcumin is a bifunctional antioxidant; it exerts antioxidant activity in a direct and an indirect way by scavenging reactive oxygen species and inducing an antioxidant response, respectively. The renoprotective effect of curcumin has been evaluated in several experimental models including diabetic nephropathy, chronic renal failure, ischemia and reperfusion and nephrotoxicity induced by compounds such as gentamicin, adriamycin, chloroquine, iron nitrilotriacetate, sodium fluoride, hexavalent chromium and cisplatin. It has been shown recently in a model of chronic renal failure that curcumin exerts a therapeutic effect; in fact it reverts not only systemic alterations but also glomerular hemodynamic changes. Another recent finding shows that the renoprotective effect of curcumin is associated to preservation of function and redox balance of mitochondria. Taking together, these studies attribute the protective effect of curcumin in the kidney to the induction of the master regulator of antioxidant response nuclear factor erythroid-derived 2 (Nrf2), inhibition of mitochondrial dysfunction, attenuation of inflammatory response, preservation of antioxidant enzymes and prevention of oxidative stress. The information presented in this paper identifies curcumin as a promising renoprotective molecule against renal injury.

Show MeSH
Related in: MedlinePlus