Naringenin confers protection against oxidative stress through upregulation of Nrf2 target genes in cardiomyoblast cells

Ramprasath, Tharmarajan; Manivasagam, Senthamizharasi; Vasudevan, Varadaraj; Sundaresan, Sivapatham; Sambandam, Yuvaraj; Selvam, Govindan Sadasivam

doi:10.1007/s13105-014-0318-3

Cited by 54 publications

(38 citation statements)

References 24 publications

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“…This indicates that naringenin exerts antiapoptotic effect, which can be attributed to its anti-inflammatory, antioxidant, and antinitrosative properties. Similarly, other studies showed that caspase-3 and cell apoptosis were significantly inhibited by naringenin [32,33] .…”

Section: Discussionmentioning

confidence: 56%

Protective Effect of Naringenin against Lipopolysaccharide-Induced Acute Lung Injury in Rats

Fouad

Albuali²,

Jresat³

2016

Pharmacology

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Background/Aims: Lipopolysaccharide (LPS) induces acute lung injury (ALI) through oxidative stress and inflammation. Naringenin exerts antioxidant and anti-inflammatory effects. The possible protective effect of naringenin was investigated against ALI induced by LPS in rats. Methods: Rats received a single injection of LPS (5 mg/kg, i.v.). Naringenin was given for 4 consecutive days, at 2 doses (50 and 100 mg/kg/day, p.o.), starting 3 days before LPS administration. Results: LPS significantly increased wet/dry lung weight ratio, malondialdehyde, nitric oxide (NO), interleukin-6, and myeloperoxidase activity in the lung tissues. Naringenin, particularly the higher dose, significantly ameliorated the LPS-induced changes in the measured parameters. Also, naringenin markedly reduced the histopathological lung tissue injury that resulted from LPS. Naringenin significantly decreased the LPS-induced expression of nuclear factor-κB, inducible NO synthase, tumor necrosis factor-a, caspase-3, and significantly increased heat shock protein 70 expression in the lungs. Conclusion: Naringenin significantly protected against LPS-induced ALI in rats through its anti-inflammatory, antioxidant, antinitrosative, and antiapoptotic effects.

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Section: Discussionmentioning

confidence: 56%

Protective Effect of Naringenin against Lipopolysaccharide-Induced Acute Lung Injury in Rats

Fouad

Albuali²,

Jresat³

2016

Pharmacology

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“…In agreement with previous reports[13,15,50-53], CCl 4 decreased GPx activity in this study. NAR cotreatment partially prevented the decrement in GPx activity, probably by up regulating its expression through Nrf2 modulation[15,40,43,44-47,50], providing another mechanism to fight oxidative stress induced by CCl 4 .…”

Section: Discussionmentioning

confidence: 99%

Naringenin prevents experimental liver fibrosis by blocking TGFβ-Smad3 and JNK-Smad3 pathways

Hernández-Aquino

Zarco

Casas‐Grajales

et al. 2017

WJG

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AIMTo study the molecular mechanisms involved in the hepatoprotective effects of naringenin (NAR) on carbon tetrachloride (CCl4)-induced liver fibrosis.METHODSThirty-two male Wistar rats (120-150 g) were randomly divided into four groups: (1) a control group (n = 8) that received 0.7% carboxy methyl-cellulose (NAR vehicle) 1 mL/daily p.o.; (2) a CCl4 group (n = 8) that received 400 mg of CCl4/kg body weight i.p. 3 times a week for 8 wk; (3) a CCl4 + NAR (n = 8) group that received 400 mg of CCl4/kg body weight i.p. 3 times a week for 8 wk and 100 mg of NAR/kg body weight daily for 8 wk p.o.; and (4) an NAR group (n = 8) that received 100 mg of NAR/kg body weight daily for 8 wk p.o. After the experimental period, animals were sacrificed under ketamine and xylazine anesthesia. Liver damage markers such as alanine aminotransferase (ALT), alkaline phosphatase (AP), γ-glutamyl transpeptidase (γ-GTP), reduced glutathione (GSH), glycogen content, lipid peroxidation (LPO) and collagen content were measured. The enzymatic activity of glutathione peroxidase (GPx) was assessed. Liver histopathology was performed utilizing Masson’s trichrome and hematoxylin-eosin stains. Zymography assays for MMP-9 and MMP-2 were carried out. Hepatic TGF-β, α-SMA, CTGF, Col-I, MMP-13, NF-κB, IL-1, IL-10, Smad7, Smad3, pSmad3 and pJNK proteins were detected via western blot.RESULTSNAR administration prevented increases in ALT, AP, γ-GTP, and GPx enzymatic activity; depletion of GSH and glycogen; and increases in LPO and collagen produced by chronic CCl4 intoxication (P < 0.05). Liver histopathology showed a decrease in collagen deposition when rats received NAR in addition to CCl4. Although zymography assays showed that CCl4 produced an increase in MMP-9 and MMP-2 gelatinase activity; interestingly, NAR administration was associated with normal MMP-9 and MMP-2 activity (P < 0.05). The anti-inflammatory, antinecrotic and antifibrotic effects of NAR may be attributed to its ability to prevent NF-κB activation and the subsequent production of IL-1 and IL-10 (P < 0.05). NAR completely prevented the increase in TGF-β, α-SMA, CTGF, Col-1, and MMP-13 proteins compared with the CCl4-treated group (P < 0.05). NAR prevented Smad3 phosphorylation in the linker region by JNK since this flavonoid blocked this kinase (P < 0.05).CONCLUSIONNAR prevents CCl4 induced liver inflammation, necrosis and fibrosis, due to its antioxidant capacity as a free radical inhibitor and by inhibiting the NF-κB, TGF-β-Smad3 and JNK-Smad3 pathways.

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“…Indeed NGN (50 µM) protected H9c2 cardiomyocytes from H 2 O 2 -mediated cells death, reduced lipid peroxidation and increased the activity of anti-oxidant enzymes [81]. …”

Section: In Vitro Effects Of Polyphenols Against Oxidative Stress-mentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

et al. 2017

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Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.

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Naringenin confers protection against oxidative stress through upregulation of Nrf2 target genes in cardiomyoblast cells

Cited by 54 publications

References 24 publications

Protective Effect of Naringenin against Lipopolysaccharide-Induced Acute Lung Injury in Rats

Protective Effect of Naringenin against Lipopolysaccharide-Induced Acute Lung Injury in Rats

Naringenin prevents experimental liver fibrosis by blocking TGFβ-Smad3 and JNK-Smad3 pathways

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

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