Dietary (–)-epicatechin mitigates oxidative stress, NO metabolism alterations, and inflammation in renal cortex from fructose-fed rats

Prince, Paula D.; Lanzi, Cecilia Rodríguez; Toblli, Jorge Eduardo; Elesgaray, Rosana; Oteiza, Patricia I.; Fraga, César G.; Galleano, Mónica

doi:10.1016/j.freeradbiomed.2015.11.009

Cited by 77 publications

(61 citation statements)

References 57 publications

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“…Our results are compatible with the hypothesis that (−)-epicatechin downregulates LPS-induced NOX activity by translational and post-translational modifications. For NOX2, (−)-epicatechin prevented the increase in the expression of the modulating protein p47 phox ; agreeing with previous reports [31], [44], but did not affect the increased expression in the catalytic subunit (gp91 phox ). For NOX4, the effect of (−)-epicatechin was on the expression of the catalytic subunit.…”

Section: Discussionsupporting

confidence: 92%

“…For NOX4, the effect of (−)-epicatechin was on the expression of the catalytic subunit. A similar pattern for the expression of NOX subunits was observed in the kidney cortex of fructose-fed rats treated with (−)-epicatechin [31]. Then, it can be concluded that the actions of (−)-epicatechin on oxidant metabolism in the kidney are more related to limiting oxidant production than to scavenging already formed radicals.…”

Section: Discussionsupporting

confidence: 64%

“…Comparable anti-inflammatory actions have been previously reported in several in vivo models of endotoxemia when using flavonoid-rich plant extracts, as well as for isolated flavonoids or their metabolites [25], [26], [27], [28], [29]. Regarding the actions of ( − )-epicatechin, we have previously reported that in fructose-fed and in high fat-fed rats inflammatory markers were mostly normalized by the presence of (−)-epicatechin in the diet [30], [31]. Then, the present results are confirmatory of an anti-inflammatory action of (−)-epicatechin, in this case associated with improved kidney function.…”

Section: Discussionmentioning

confidence: 57%

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LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

et al. 2017

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This work investigated the capacity of (−)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80 mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (LPS). Six hours after injection, LPS-treated rats exhibited increased plasma creatinine and urea levels as indicators of impaired renal function. The renal cortex of the LPS-treated rats showed: i) increased expression of inflammatory molecules (TNF-α, iNOS and IL-6); ii) activation of several steps of NF-κB pathway; iii) overexpression of TLR4, and iv) higher superoxide anion production and lipid peroxidation index in association with increased levels of gp91phox and p47phox (NOX2) and NOX4. Pretreatment with dietary (−)-epicatechin prevented the adverse effects of LPS challenge essentially by inhibiting TLR4 upregulation and NOX activation and the consequent downstream events, e.g. NF-kB activation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 57%

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LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

et al. 2017

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“…These findings support other studies in which the antioxidant capacity of Epi was associated either with activation of the enzymes involved in the antioxidant defense system [42] in the heart or with radical-scavenging properties in endothelial cells without affecting NADPH oxidase activity in vitro [43, 44]. On the other hand, short-term Epi cotreatment reduced protein expression levels of the p47phox subunit of NADPH oxidase in the hearts of rats with L-NAME-induced hypertension [24] and in the renal cortex in fructose-fed rats [45], in contrast to our findings in a genetic model of hypertension. Regarding nitrosative damage, in vitro studies revealed that Epi protected cells against peroxynitrite-induced damage [46, 47] similarly as we observed in vivo in blood.…”

Section: Discussionmentioning

confidence: 99%

(−)-Epicatechin Prevents Blood Pressure Increase and Reduces Locomotor Hyperactivity in Young Spontaneously Hypertensive Rats

Kluknavsky

Bališ

Púzserová

et al. 2016

Oxidative Medicine and Cellular Longevity

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This study investigated the effects of subchronic (−)-epicatechin (Epi) treatment on locomotor activity and hypertension development in young spontaneously hypertensive rats (SHR). Epi was administered in drinking water (100 mg/kg/day) for 2 weeks. Epi significantly prevented the development of hypertension (138 ± 2 versus 169 ± 5 mmHg, p < 0.001) and reduced total distance traveled in the open-field test (22 ± 2 versus 35 ± 4 m, p < 0.01). In blood, Epi significantly enhanced erythrocyte deformability, increased total antioxidant capacity, and decreased nitrotyrosine concentration. In the aorta, Epi significantly increased nitric oxide (NO) synthase (NOS) activity and elevated the NO-dependent vasorelaxation. In the left heart ventricle, Epi increased NOS activity without altering gene expressions of nNOS, iNOS, and eNOS. Moreover, Epi reduced superoxide production in the left heart ventricle and the aorta. In the brain, Epi increased nNOS gene expression (in the brainstem and cerebellum) and eNOS expression (in the cerebellum) but had no effect on overall NOS activity. In conclusion, Epi prevented the development of hypertension and reduced locomotor hyperactivity in young SHR. These effects resulted from improved cardiovascular NO bioavailability concurrently with increased erythrocyte deformability, without changes in NO production in the brain.

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“…Ratlarda yüksek fruktoz tüketimiyle oluşturulmuş renal hasara epikateşinin etkisinin araştırıldığı bir çalışmada; fruktoz tüketimiyle yükselen TNFα, indüklenebilir nitrik oksit sentaz (iNOS), ve IL-6 düzeyleri, fruktozla birlikte epikateşin tüketen grupta anlamlı oranda düşmüştür. Bu nedenle inflamasyonla ilişkili böbrek hasarında epikateşin suplementasyonunun olumlu etkileri olabileceği sonucuna varılmıştır (91).…”

Section: Türk Nefroloji Diyaliz Ve Transplantasyon Dergisi Turkish Neunclassified

Kronik Böbrek Hastalığında Renal İnflamasyon ve Bazı Güncel Diyet Bileşenleri İlişkisi

Öztürk¹,

Nergiz-Unal²

2018

Turk Neph Dial Transpl

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ÖZKronik böbrek hastalığı, glomerüler filtrasyonun azalmasıyla böbrekte sıvı-solüt dengesinin düzenlen-mesi ve metabolik-endokrin fonksiyonlarda kronik ve ilerleyici bozulma hali olarak tanımlanabilir. Kronik böbrek hastalığı gelişiminde rol alan inflamasyon, kronik böbrek hastalığının sonucu olarak da ortaya çıkabilmekte ve KBH varlığına bağlı mortalite artışının en önemli nedenlerinden biri olarak kabul edilmektedir. İnflamasyon ve diyet etkileşimi ile ilgili yapılan güncel araştırmalar çoklu doymamış yağ asitleri, D vitamini, E vitamini gibi besin ögeleri ile karnitin, lipoik asit, flavanoidler, probiyotikler ve prebiyotikler gibi diğer diyet bileşenlerinin renal inflamasyon sürecindeki olumlu etkilerine işaret etmektedir. Derlemede, olası anti-inflamatuvar bazı diyet bileşenlerinin kronik böbrek hastalığı ile ilişkili inflamasyon üzerine etkileri incelenmiştir. ANAHTAR SÖZCÜKLER: Kronik böbrek hastalığı, Beslenme, İnflamasyon, Diyet ABSTRACTChronic kidney disease can be defined as chronic and progressive deterioration of the regulation of fluid-solute balance and metabolic-endocrine functions of the kidney due to diminishing glomerular filtration. Inflammation in renal disease can develop as a cause or an outcome, and it has been reported in recent studies that inflammation is among the most important causes of disease-related mortality. Investigations on inflammation and diet interactions have shown that the effects of nutrients such as polyunsaturated fatty acids, vitamin D, vitamin E and other dietary components such as carnitine, lipoic acid, flavanoids, probiotics and prebiotics may have positive effects on the renal inflammation process. In this review, the potential anti-inflammatory effects of some current dietary components in chronic kidney disease were studied.

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Dietary (–)-epicatechin mitigates oxidative stress, NO metabolism alterations, and inflammation in renal cortex from fructose-fed rats

Cited by 77 publications

References 57 publications

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

(−)-Epicatechin Prevents Blood Pressure Increase and Reduces Locomotor Hyperactivity in Young Spontaneously Hypertensive Rats

Kronik Böbrek Hastalığında Renal İnflamasyon ve Bazı Güncel Diyet Bileşenleri İlişkisi

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