Nrf2

Kim, K.M.; Ki, Sung Hwan

doi:10.1016/b978-0-12-804274-8.00028-x

Cited by 15 publications

(12 citation statements)

References 214 publications

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“…It is noticeable that the capacity of stevia leaves to improve the functional markers of acute liver damage is paralleled by its ability to prevent the changes in the markers of oxidative stress produced by acute CCl 4 intoxication. In this regard, it is well known that free radicals play an important causative role in liver diseases [ 10 , 29 , 36 – 38 ]. These results prompted us to investigate the antioxidant and hepatoprotective properties of stevia on chronic liver damage produced by this hepatotoxic compound.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, it is noteworthy that stevia treatment of CCl 4 -treated animals resulted in the prevention of oxidative markers such as MDA, GSH, GPx, and 4-HNE. Thus, these results prompted us to investigate whether stevia leaves could induce the expression of Nrf2, a key regulator of redox signaling in the liver [ 37 , 38 ]. Chronic CCl 4 treatment resulted in decreased expression of Nrf2 in the livers.…”

Section: Discussionmentioning

confidence: 99%

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Stevia Prevents Acute and Chronic Liver Injury Induced by Carbon Tetrachloride by Blocking Oxidative Stress through Nrf2 Upregulation

Ramos‐Tovar

Hernández-Aquino

Casas‐Grajales

et al. 2018

Oxidative Medicine and Cellular Longevity

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The effect of stevia on liver cirrhosis has not been previously investigated. In the present study, the antioxidant and anti-inflammatory properties of stevia leaves were studied in male Wistar rats with carbon tetrachloride- (CCl4-) induced acute and chronic liver damage. Acute and chronic liver damage induced oxidative stress, necrosis, and cholestasis, which were significantly ameliorated by stevia. Chronic CCl4 treatment resulted in liver cirrhosis, as evidenced by nodules of hepatocytes surrounded by thick bands of collagen and distortion of the hepatic architecture, and stevia significantly prevented these alterations. Subsequently, the underlying mechanism of action of the plant was analyzed. Our study for the first time shows that stevia upregulated Nrf2, thereby counteracting oxidative stress, and prevented necrosis and cholestasis through modulation of the main proinflammatory cytokines via NF-κB inhibition. These multitarget mechanisms led to the prevention of experimental cirrhosis. Given the reasonable safety profile of stevia, our results indicated that it may be useful for the clinical treatment of acute and chronic liver diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Stevia Prevents Acute and Chronic Liver Injury Induced by Carbon Tetrachloride by Blocking Oxidative Stress through Nrf2 Upregulation

Ramos‐Tovar

Hernández-Aquino

Casas‐Grajales

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…NF-E2-related factor 2 (Nrf2) is an important transcription factor that controls a range of detoxifying and antioxidant protective gene expressions in the liver and is activated in response to oxidative stress and induces the expression of its target genes through binding to the antioxidant response element (ARE) (Kim & Ki, 2017).…”

Section: F I G U R Ementioning

confidence: 99%

Effects of walnut oil on metabolic profile and transcription factors in rats fed high‐carbohydrate‐/‐fat diets

et al. 2020

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The aim of this study was to examine the effects of walnut oil (WO) on metabolic profile and transcription factors in rats fed high carbohydrate (HCD) and high‐fat diet (HFD). Forty‐two male rats were divided in to six groups: (a) Control, (b) WO (20 mg/kg BW), (c) HCD (20% of sucrose), (d) HCD + WO (e) HFD (42% of calories as fat), and (f) HFD + WO. HFD and HCD intake increased final body weights by 19% and 23% and visceral fat weights by 3‐ and 5‐fold, respectively (p < .05 for all). In addition, serum glucose, total cholesterol, triglyceride, and free fatty acids (FFA) insulin, leptin, and MDA levels increased in rats fed with HFD and HCD. WO supplementation improved these metabolic parameters (p < .05 for all). HFD + WO and HCD + WO treated groups had a significant reduction in serum and liver malondialdehyde (MDA) levels by 12% or 15% (p < .05 for both). In addition, WO supplementation lowered the levels of hepatic nuclear factor kappa B (NF‐κB) and NADPH oxidase subunit p22phox, whereas increased the endothelial‐NO synthase (e‐NOS), nuclear factor erythroid 2‐related factor‐2, and sirtuin‐1 levels. In conclusion, WO supplementation could alleviate the adverse impacts of both HCD and HFD in the rats. Practical applications This study suggests that WO intake can modulate carbohydrate metabolism and increase antioxidant capacity. These properties might be partially mediated through the regulation of the transcription factors and some proteins involved in energy metabolism, as well as a balance of oxidative stress, and insulin sensitivity.

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“…In high oxidative stress conditions, p53 acts as a prooxidant, increasing expression of prooxidative genes, such as proline oxidase, to initiate a stress cascade that ultimately leads to cell death [ 102 ]. In parallel to its upregulation of prooxidative genes, p53 inhibits nuclear factor E2-related factor 2 (Nrf2), a critical antioxidant transcription factor [ 103 ], ultimately repressing the expression of genes involved in glutathione metabolism (namely, GCLM, GCLC, GR , and cysteine transporter SLC7A11 ) [ [104] , [105] , [106] ]. SLC7A11, also referred to as xCT , is the regulator of intracellular cysteine, the essential rate-limiting precursor to GSH biosynthesis [ 86 , 87 , 107 , 108 ].…”

Section: Discussionmentioning

confidence: 99%

Quantitative trait mapping in Diversity Outbred mice identifies novel genomic regions associated with the hepatic glutathione redox system

et al. 2021

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The tripeptide glutathione (GSH) is instrumental to antioxidant protection and xenobiotic metabolism, and the ratio of its reduced and oxidized forms (GSH/GSSG) indicates the cellular redox environment and maintains key aspects of cellular signaling. Disruptions in GSH levels and GSH/GSSG have long been tied to various chronic diseases, and many studies have examined whether variant alleles in genes responsible for GSH synthesis and metabolism are associated with increased disease risk. However, past studies have been limited to established, canonical GSH genes, though emerging evidence suggests that novel loci and genes influence the GSH redox system in specific tissues. The present study marks the most comprehensive effort to date to directly identify genetic loci associated with the GSH redox system. We employed the Diversity Outbred (DO) mouse population, a model of human genetics, and measured GSH and the essential redox cofactor NADPH in liver, the organ with the highest levels of GSH in the body. Under normal physiological conditions, we observed substantial variation in hepatic GSH and NADPH levels and their redox balances, and discovered a novel, significant quantitative trait locus (QTL) on murine chromosome 16 underlying GSH/GSSG; bioinformatics analyses revealed Socs1 to be the most likely candidate gene. We also discovered novel QTL associated with hepatic NADP + levels and NADP + /NADPH, as well as unique candidate genes behind each trait. Overall, these findings transform our understanding of the GSH redox system, revealing genetic loci that govern it and proposing new candidate genes to investigate in future mechanistic endeavors.

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Nrf2

Cited by 15 publications

References 214 publications

Stevia Prevents Acute and Chronic Liver Injury Induced by Carbon Tetrachloride by Blocking Oxidative Stress through Nrf2 Upregulation

Stevia Prevents Acute and Chronic Liver Injury Induced by Carbon Tetrachloride by Blocking Oxidative Stress through Nrf2 Upregulation

Effects of walnut oil on metabolic profile and transcription factors in rats fed high‐carbohydrate‐/‐fat diets

Quantitative trait mapping in Diversity Outbred mice identifies novel genomic regions associated with the hepatic glutathione redox system

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