Resveratrol Ameliorates Contrast Induced Nephropathy Through the Activation of SIRT1-PGC-1α-Foxo1 Signaling in Mice

Hong, Yu Ah; Bae, So Yeon; Ahn, Shin Young; Kim, Jieun; Kwon, Young Joo; Jung, Woon Yong; Ko, Gang Jee

doi:10.1159/000481804

Cited by 32 publications

(46 citation statements)

References 45 publications

(47 reference statements)

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“…In NRK-52E rodent tubular cells, CM caused oxidative stress and decreased cell viability by downregulation of SIRT1 [21]. Transfection with SIRT1 siRNA resulted in increased apoptosis in these cells treated with CM [21]. These findings indicated that CM downregulated SIRT1, leading to increased cell apoptosis ( Table 1).…”

Section: Roles Of Silent Information Regulator 1 (Sirt1) In Cinmentioning

confidence: 91%

“…SIRT1 is a histone deacetylase of nicotinamide adenine dinucleotide (NAD + ), which mainly exists in the nucleus [20]. In NRK-52E rodent tubular cells, CM caused oxidative stress and decreased cell viability by downregulation of SIRT1 [21]. Transfection with SIRT1 siRNA resulted in increased apoptosis in these cells treated with CM [21].…”

Section: Roles Of Silent Information Regulator 1 (Sirt1) In Cinmentioning

confidence: 99%

“…In mice, CM administration activated the Nox4/Nox2 axis, resulting in increased ROS production, and involving the MAPK pathway (including p38, JNK and ERK pathways) resulting in apoptosis, leading to impaired renal function [17]. CM administration also downregulated SIRT1 and upregulated peroxisome proliferator-activated receptor gamma-assisted activating factor-1α-Forkhead-box transcription factor 1 (PGC-1α-FoxO1) signaling mediated oxidative stress and apoptosis, leading to impaired renal function (Table 2) [21].…”

Section: Roles Of Mapk and Sirt1 In Cinmentioning

confidence: 99%

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Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

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Section: Roles Of Silent Information Regulator 1 (Sirt1) In Cinmentioning

confidence: 91%

Section: Roles Of Silent Information Regulator 1 (Sirt1) In Cinmentioning

confidence: 99%

Section: Roles Of Mapk and Sirt1 In Cinmentioning

confidence: 99%

See 1 more Smart Citation

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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“…In diabetic peripheral neuropathy, overexpression of Sirt1 can increase axonal growth through Sirt1/ PGC-1α/ TFAM axis and improve mitochondrial oxidative metabolism (40). It has also been shown that Sirt1/PGC-1α signaling pathway can further regulate the role of uncoupling protein 2(UCP2) or Forkhead box protein O1(FOXO1) in reducing oxidative stress and neuronal apoptosis (41,42). In our study, decreasing Sirt1 reduced the expression of PGC-1α and increased apoptosis, resulting in intracellular increased MDA and decreased SOD, which are related to cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Sirt1 Regulates Oxidative Stress in Oxygen-Glucose Deprived Hippocampal Neurons

et al. 2020

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Oxidative stress is an important mechanism of neonatal hypoxic-ischemic brain damage. Sirtuin1 (Sirt1) is a deacetylase that depends on NAD + , which has an important role in antioxidant metabolism. Furthermore, peroxisome proliferator-activated receptor γ-co-activator 1α (PGC-1α) is a key regulator of mitochondrial oxidative stress, which is regulated by Sirt1. Here, we investigated the role of Sirt1 in the pathogenesis of brain injuries after modulating its activity in primary cultured hippocampal neurons. Our study shows that the expression of Sirt1 was downregulated after oxygen-glucose deprivation. Activation of Sirt1 with resveratrol improved cell's resistance to oxidative stress, whereas inhibition of Sirt1 with EX527 significantly reduced cell viability after cellular oxidative stress. Our study also shows that activation of Sirt1 with resveratrol exerts its antioxidant effect by regulating the expression of PGC-1α. In contrast, application of EX527 decreased the expression of PGC-1α. In summary, these results confirmed that Sirt1 is a potent protective factor for neurons subjected to oxidative stress, and the protective effect of Sirt1 is attributed to its regulation of PGC-1α.

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“…Notably, FOXO1 siRNA transfection reduced the protein expression of p-mTOR in PA-treated HK-2 cells, which may explain the finding that no more MCP-1 was expressed in the PA+FOXO1 siRNA group compared with the PA group. Recently, certain reports have suggested a role for FOXO1 in renal protection (27,28). However, further investigation is required to explore whether FOXO1 is beneficial or detrimental in kidney diseases.…”

Section: Discussionmentioning

confidence: 99%

Role of the mTOR‑FOXO1 pathway in obesity‑associated renal tubulointerstitial inflammation

Sun

Shao

et al. 2018

Mol Med Report

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Since obesity is largely responsible for the growing incidence of renal tubulointerstitial inflammation, exploration into the mechanisms of obesity-associated tubulointerstitial inflammation is essential. Studies have demonstrated that mammalian target of rapamycin (mTOR) is a crucial molecule in the pathogenesis of renal inflammation, including regulating the expression of inflammatory factors. The purpose of the present study was to further elucidate the role of mTOR in obesity-associated tubulointerstitial inflammation. In the clinical study, obese and healthy subjects were recruited for physical examination, as well as the collection of blood and urine samples. Further study was performed on a high fat diet (HFD)-induced obese rat model and a cultured human renal tubular epithelial cell line (HK-2). The clinical study demonstrated that the participants with obesity had increased serum lipids, creatinine (Cr), urinary albumin to creatinine ratio (UACR) and urinary neutrophil gelatinase-associated lipocalin (u-NGAL). Moreover, the level of urinary monocyte chemoattractant protein-1 (u-MCP-1) was increased in the participants with obesity, and it was positively correlated with free fatty acid (FFA), UACR and u-NGAL. In the in vivo study, the results indicated that the levels of serum lipids, Cr and blood urea nitrogen (BUN), as well as 24 h urine protein and u-NGAL, were significantly increased in the HFD-fed obese rats. In addition, the infiltration of CD68 + cells into the renal interstitial area and the release of interleukin-1β (IL-1β) was observed in the kidneys of obese rats. Meanwhile, the supernatant from HK-2 cells treated with palmitic acid stimulated THP-1 monocyte migration. The upregulation of MCP-1, phosphorylated forkhead boxO1 (p-FOXO1), and phosphorylated mTOR (p-mTOR) was observed in vivo and in vitro. However, inhibition of mTOR was able to alleviate the above effects. Overall, these results demonstrated that activated mTOR induced FOXO1 phosphorylation, which mediates renal MCP-1 release, causes tubulointerstitial inflammation and ultimately leads to pathological renal changes and dysfunction. However, inhibition of mTOR may play a renoprotective role during the progression of obesity-associated tubulointerstitial inflammation.

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Resveratrol Ameliorates Contrast Induced Nephropathy Through the Activation of SIRT1-PGC-1α-Foxo1 Signaling in Mice

Cited by 32 publications

References 45 publications

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Sirt1 Regulates Oxidative Stress in Oxygen-Glucose Deprived Hippocampal Neurons

Role of the mTOR‑FOXO1 pathway in obesity‑associated renal tubulointerstitial inflammation

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