Sodium butyrate decreases the activation of NF- B reducing inflammation and oxidative damage in the kidney of rats subjected to contrast-induced nephropathy

Machado, Roberta; Constantino, Larissa; Tomasi, Cristiane Damiani; Rojas, Hugo; Vuolo, Francieli; Vitto, Marcelo F.; Cesconetto, Patrícia Acordi; Souza, Cláudio Teodoro de; Ritter, Cristiane

doi:10.1093/ndt/gfr807

Cited by 116 publications

(90 citation statements)

References 22 publications

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“…Other studies have observed a reduction in kidney injury in other models after SCFA treatment. 22,23 The higher protection observed after acetate treatment might be due to the composition of acetate, favoring the rapid entry of the molecule into the metabolic pathway, whereas other types of SCFAs need to Figure 6. SCFA treatment inhibits NFkb activation and nitric oxide production in epithelial kidney cell line.…”

Section: Discussionmentioning

confidence: 99%

“…Acetate administration can also protect from colitis in the absence of microbiota, 15 whereas the administration of SCFAs in wild-type mice also protects from other diseases. 17,22,23 Despite the importance of the presence of microbiota in maintaining intestinal homeostasis 39 and preventing inflammation, it appears that an increase in the concentration of SCFAs could enhance this protection. It is already known that gut microbiota can change composition rapidly through diet alteration.…”

Section: Discussionmentioning

confidence: 99%

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Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Andrade-Oliveira

Amano

Corrêa-Costa

et al. 2015

Journal of the American Society of Nephrology

402

330

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Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase-inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4 + and CD8 + T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Andrade-Oliveira

Amano

Corrêa-Costa

et al. 2015

Journal of the American Society of Nephrology

402

330

View full text Add to dashboard Cite

show abstract

“…In contrast, treating Npr1 ϩ/Ϫ mice with RA and SB alone or in combination prevented the expression of matrix synthesis in the cardiac tissue, suggesting that these drugs exert protective effects over the matrix remodeling process. NF-B is a redox-sensitive transcription factor that directly regulates the expression of immediate-to earlyresponse genes, cytokines, and inflammatory molecules (38,73). It has been shown that NF-B activity is significantly increased in vitamin A-deficient mice, while RA treatment attenuates its increased activation (2).…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice

Umadevi

Kumar

Mani

et al. 2016

Physiological Genomics

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“…Many stimuli relevant to kidney injury can activate NF-κB, such as high glucose, advanced glycosylation end products, cytokines, growth factors, toll-like receptors and proteinuria. Large amounts of experimental results have demonstrated that inhibition of NF-κB ameliorates inflammation, conferring a renoprotective phenotype (70)(71)(72)(73)(74).…”

Section: Sirt1 Suppresses Inflammation By Targeting Nf-κb and High-momentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

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Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

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Sodium butyrate decreases the activation of NF- B reducing inflammation and oxidative damage in the kidney of rats subjected to contrast-induced nephropathy

Abstract: The current experiment suggests that NF-κB induced an inflammatory response after CIN and SB could inhibit NF-κB expression protecting against CIN in rats.

Cited by 116 publications

References 22 publications

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice

Sirtuin 1: A Target for Kidney Diseases

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