The flavonoid monoHER promotes the adaption to oxidative stress during the onset of NAFLD

Lemmens, Kristien J.A.; Wier, Bregje van de; Koek, Ger H.; Köhler, S. Eleonore; Drittij, M.-J.; Vijgh, W.J.F. van der; Bast, Aalt; Haenen, Guido R.M.M.

doi:10.1016/j.bbrc.2014.11.055

Cited by 10 publications

(8 citation statements)

References 19 publications

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“…Induction of nuclear erythroid 2‐related factor 2, the key transcription factor involved in the induction of phase 2 enzymes, and increased expression of heme oxygenase‐1, one of the phase 2 enzymes has been observed following quercetin administration in animal models and proposed as a momentous mechanism for suppression of NAFLD‐associated lipid peroxidation by quercetin (Kim et al, ). Similarly, rutin the glycosylated form of quercetin exerted its protection against oxidative stress initiated by a high‐carbohydrate high‐cholesterol diet through induction of antioxidant enzyme genes, heme oxygenase‐1, and glutathione peroxidase 3 (Lemmens et al, ). It is interesting that rutin could appear its protection when administered subcutaneously (Lemmens et al, ).…”

Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 99%

“…Similarly, rutin the glycosylated form of quercetin exerted its protection against oxidative stress initiated by a high‐carbohydrate high‐cholesterol diet through induction of antioxidant enzyme genes, heme oxygenase‐1, and glutathione peroxidase 3 (Lemmens et al, ). It is interesting that rutin could appear its protection when administered subcutaneously (Lemmens et al, ).…”

Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 99%

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Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Akhlaghi

2016

Phytother. Res.

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Non-alcoholic fatty liver disease (NAFLD) has been known as the hepatic feature of metabolic syndrome. Extra fat depots, especially in visceral areas, develop insulin resistance as a result of mild oxidation and inflammation. Insulin resistance induces lipolysis and releases free fatty acids into the circulation, where they are transported to the liver. In the liver, free fatty acids are converted to triglycerides and accumulate, causing simple steatosis that, if left untreated, can lead to steatohepatitis, and subsequently liver necrosis and cirrhosis.Flavonoids, a group of plant compounds with incredible biological characteristics, have shown advantages in pathological conditions. Beneficial effects of flavonoids against NAFLD and its related disorders have been observed in both animal and human studies. Various mechanisms have been found for their protection. Flavonoids prevent hepatosteatosis by increasing fatty acid oxidation in the liver. They can also reduce caloric intake and decrease body weight and fat deposition in visceral tissues. Flavonoids are unique antioxidants that exert their beneficial effects through inhibition of nuclear factor κB, thereby attenuating release of inflammatory cytokines, which are triggers of insulin resistance. Finally, flavonoids have shown to increase adiponectin, improve insulin sensitivity and glucose tolerance, correct dyslipidemia, and reduce blood pressure in patients with NAFLD. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 99%

Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 99%

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Akhlaghi

2016

Phytother. Res.

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“…Oxidative stress plays a key role in causing the NAFLD process. High activity molecules such as reactive oxygen (ROS) and reactive nitrogen (RNS) free radicals caused an imbalance between prooxidant and antioxidant chemical species that led to oxidative damage of cellular macromolecules [ 37 , 38 ]. A previous study has reported that polyphenols can reduce the production of ROS and RNS [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Amelioration by Idesia polycarpa Maxim. var. vestita Diels. of Oleic Acid-Induced Nonalcoholic Fatty Liver in HepG2 Cells through Antioxidant and Modulation of Lipid Metabolism

Sun

et al. 2020

Oxidative Medicine and Cellular Longevity

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Idesia polycarpa Maxim. var. vestita Diels (I. polycarpa) is well known as an edible oil plant which contains abundant linoleic acid and polyphenols. The objective of this study was to maximize the by-product of defatted fruit of I. polycarpa. We found that the fraction D of ethyl acetate extract (EF-D) contained more polyphenols, which contribute to its strong antioxidant activity by antioxidant assays (DPPH, ABTS, and FRAP). Meanwhile, EF-D showed a significant lipid-lowering effect on oleic acid- (OA-) induced hepatic steatosis in HepG2 cells through enhancing antioxidant activity, reducing liver damage, and regulating lipid metabolism, antioxidant, and inflammation-related gene expression. The SOD and T-AOC levels significantly increased, but the levels of MDA, AST, and ALT decreased obviously when treated with EF-D. In general, EF-D improved the antioxidant enzyme activities and decreased the hepatic injury activities. Besides, treatment with EF-D for NAFLD influenced lipid metabolism and inflammation by activating PPARα which was associated with the increased expression of CPT1 and decreased expression of SCD, NF-κB, and IL-1. Moreover, EF-D improved the oxidative stress system through activation of the Nrf2 antioxidant signal pathways and upregulated its target genes of HO-1, NQO1, and GSTA2. The results highlighted the EF-D from the defatted fruit of I. polycarpa regarding lipid-lowering, proving it to be a potential drug resource of natural products for treating the nonalcoholic fatty liver disease (NAFLD).

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“…Furthermore, flavonoids have also exhibited therapeutic properties in NAFLD by enhancing cellular antioxidant protection. 27,28 Meanwhile, many flavonoids have been proven to be Nrf2-ARE activators (Table 1).…”

Section: Flavonoidsmentioning

confidence: 99%

“…7-Mono-O-(β-hydroxyethyl)rutoside (MonoHER) has been reported to activate the antioxidant defense system of Nrf2 by improving the ratio of GSH/glutathione disulfide (GSSG) and increasing the expression levels of the HO-1 and glutathione peroxidase 3 (GPx3) genes in Ldlr −/− mice. 27 Scutellarin (4′,5,6-trihydroxy flavonoid-7-glucuronide) increased the level of Nrf2 protein in C57BL/6J mice fed an HFD. Total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol in serum were reduced in groups that were fed scutellarin.…”

Section: Flavonoidsmentioning

confidence: 99%

Chemical Activators of the Nrf2 Signaling Pathway in Nonalcoholic Fatty Liver Disease

Jiang

et al. 2021

Natural Product Communications

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Nonalcoholic fatty liver disease (NAFLD) is paralleling the insulin resistance and obesity epidemic and is regarded as liver metabolic syndrome, and its prevalence rate is increasing rapidly. The best explanation for the occurrence and development of NAFLD is the “multiple hit” hypothesis instead of the “two-hit” hypothesis. At present, NAFLD therapies are limited. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is a key pathway in oxidative stress. Its downstream proteins/enzymes are regulated. Metabolic enzymes and antioxidant proteins/enzymes play a vital role in cell defense protection and have attracted attention in the field of antioxidant research in recent years. This paper summarizes the regulatory mechanism of the Nrf2 signaling pathway and the research progress of Nrf2 activators in NAFLD to provide guidance for NAFLD therapy in the future.

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The flavonoid monoHER promotes the adaption to oxidative stress during the onset of NAFLD

Cited by 10 publications

References 19 publications

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Amelioration by Idesia polycarpa Maxim. var. vestita Diels. of Oleic Acid-Induced Nonalcoholic Fatty Liver in HepG2 Cells through Antioxidant and Modulation of Lipid Metabolism

Chemical Activators of the Nrf2 Signaling Pathway in Nonalcoholic Fatty Liver Disease

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