Naringenin modulates circulatory lipid peroxidation, anti-oxidant status and hepatic alcohol metabolizing enzymes in rats with ethanol induced liver injury

Jayaraman, Jayachitra; Nalini, Namasivayam

doi:10.1111/j.1472-8206.2010.00899.x

Cited by 26 publications

(29 citation statements)

References 44 publications

(39 reference statements)

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“…NAR was able to prevent LPO due to its molecular structure; perhaps its hydroxyl groups facilitate its adherence to lipid bilayer polar groups, and its nonpolar nucleus may interact with hydrophobic tails of phospholipids, thereby reducing the deleterious effects of free radicals on membranes[12,42,43]. …”

Section: Discussionmentioning

confidence: 99%

“…In addition to its antioxidant properties as a free radical scavenger, NAR may also act though Nrf2 activation and induce endogenous antioxidant enzymes. In fact, NAR upregulates the expression of the enzyme glutamate-cysteine ligase, the rate limiting enzyme involved in de novo GSH synthesis[44-48], as well as glutathione reductase, which catalyzes the reduction of oxidized glutathione to the reduced form[15,43]. GPx detoxifies H 2 O 2 by reducing it to water and oxygen, utilizing two molecules of GSH to form GSSG in the reduction of a molecule of H 2 O 2 [49].…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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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“…It was found abundantly in Citrus species. Naringenin and hesperidin are flavonoids that present highly in C. hystrix [14] , concentrated in peels [15] . Powerful antioxidant and free radicals scavenging activity of these compounds have been noted [10,18] .…”

Section: Discussionmentioning

confidence: 99%

“…A study reported that among parts of the plant, highest yield of extraction was obtained from peels [14] . Antioxidant activity and free radicals scavenging properties of naringenin and hesperidin have been examined by numerous researchers using various assay systems [15,16] . Naringenin could increase CD 4+ / CD 8+ ratio on T cell which is responsible for immune system [17] , while hesperidin could enhance innate and adaptive immune system [18] , and cardioprotective effect on doxorubicin induced rats [19] .…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective and hepatoprotective effects of Citrus hystrix peels extract on rats model

Putri

Nagadi

Larasati

et al. 2013

Asian Pacific Journal of Tropical Biomedicine

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Naringenin inhibits osteoclastogenesis through modulation of helper T cells‐secreted IL‐4

Wang

Luo

et al. 2017

J of Cellular Biochemistry

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Naringenin (NAR) is a natural predominant flavanone and has a wide range of pharmacological activities. The aim of this study was to investigate the protective mechanisms of NAR on RANKL-induced osteoclastogenesis and osteoclast bone resorption. T cells were divided into four groups under different concentrations of NAR (0, 25, 50, 100 µM). CD4 T cell subsets in different groups were evaluated by flow cytometry. TRAP staining, pit formation assays and F-actin ring immunofluorescent staining were performed. In addition, gene expression of osteoclast-specific markers was analyzed by qPCR and Western blot. Our results showed that compared with the control group, there were relatively fewer Th1 and Th17 cells and more Th2 cells and Treg cells in the NAR groups. Besides, the number of TRAP-positive multinucleated osteoclasts, the areas of bone resorption pits and the size and number of F-actin rings were notably decreased in the bone marrow macrophages (BMMs) treated with T-cell supernatant containing NAR. Moreover, NAR treatment dramatically reduced the expressions of cathepsin K, c-Fos, DC-STAMP, NFATc1, TRAP, and V-ATPase d2 at mRNA and protein levels. However, these effects were abolished by adding a neutralizing antibody against IL-4. In conclusion, NAR suppressed RANKL-induced osteoclastogenesis and osteoclast bone resorption by promoting the release of IL-4 from T cells.

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Naringenin modulates circulatory lipid peroxidation, anti-oxidant status and hepatic alcohol metabolizing enzymes in rats with ethanol induced liver injury

Cited by 26 publications

References 44 publications

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

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

Cardioprotective and hepatoprotective effects of Citrus hystrix peels extract on rats model

Naringenin inhibits osteoclastogenesis through modulation of helper T cells‐secreted IL‐4

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