Naringenin ameliorates daunorubicin induced nephrotoxicity by mitigating AT1R, ERK1/2-NFκB p65 mediated inflammation

Karuppagounder, Vengadeshprabhu; Arumugam, Somasundaram; Thandavarayan, Rajarajan Amirthalingam; Pitchaimani, Vigneshwaran; Sreedhar, Remya; Afrin, Rejina; Harima, Meilei; Sano, Hiroshi; Suzuki, Kenji; Nakamura, Masahiko; Ueno, K.; Watanabe, Kenichi

doi:10.1016/j.intimp.2015.05.050

Cited by 47 publications

(28 citation statements)

References 40 publications

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“…Naringenin also inhibits inflammation by targeting cyclooxygenase (COX)-2 in ethanol-induced liver injury [ 18 ] and in vitro [ 19 ]. Moreover, naringenin inhibits phosphorylation of nuclear factor kappaB (NFκB) subunit p65 and mitogen-activated protein kinases (MAPK) in daunorubicin-induced nephrotoxicity [ 20 ] as well as inhibiting the EGFR-PI3K-Akt/ERK MAPK signaling pathway in human airway epithelial cells [ 21 ]. Naringenin also inhibits a number of aspects of oxidative stress, including lipid peroxidation and O 2 − production, as well as restoring GSH levels in UVB-induced oxidative stress in the skin of Hairless mice [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Naringenin Inhibits Superoxide Anion-Induced Inflammatory Pain: Role of Oxidative Stress, Cytokines, Nrf-2 and the NO−cGMP−PKG−KATPChannel Signaling Pathway

et al. 2016

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In the present study, the effect and mechanism of action of the flavonoid naringenin were evaluated in superoxide anion donor (KO2)-induced inflammatory pain in mice. Naringenin reduced KO2-induced overt-pain like behavior, mechanical hyperalgesia, and thermal hyperalgesia. The analgesic effect of naringenin depended on the activation of the NO−cGMP−PKG−ATP-sensitive potassium channel (KATP) signaling pathway. Naringenin also reduced KO2-induced neutrophil recruitment (myeloperoxidase activity), tissue oxidative stress, and cytokine production. Furthermore, naringenin downregulated KO2-induced mRNA expression of gp91phox, cyclooxygenase (COX)-2, and preproendothelin-1. Besides, naringenin upregulated KO2-reduced nuclear factor (erythroid-derived 2)-like 2 (Nrf2) mRNA expression coupled with enhanced heme oxygenase (HO-1) mRNA expression. In conclusion, the present study demonstrates that the use of naringenin represents a potential therapeutic approach reducing superoxide anion-driven inflammatory pain. The antinociceptive, anti-inflammatory and antioxidant effects are mediated via activation of the NO−cGMP−PKG−KATP channel signaling involving the induction of Nrf2/HO-1 pathway.

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Section: Introductionmentioning

confidence: 99%

Naringenin Inhibits Superoxide Anion-Induced Inflammatory Pain: Role of Oxidative Stress, Cytokines, Nrf-2 and the NO−cGMP−PKG−KATPChannel Signaling Pathway

et al. 2016

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“…The incidence of inflammation, which is relevant in renal, neural, intestinal and pulmonary diseases, has increased in the last decade [36][37][38]. Recent studies indicate that physiologically active substances such as naringenin, exhibit an anti-nephrotoxic effects by reducing the inflammation and oxidative stress [39]. Moreover, bioconversion mediated increments in the amount of quercetin, the main antioxidant component, enhanced the anti-oxidant activity physiologically [27].…”

Section: Discussionmentioning

confidence: 99%

Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Kim

Lee

Chon

et al. 2019

JABC

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Mitogen-activated protein (MAP) kinases play an important role in cell growth and differentiation, as well as the modulation of proinflammatory cytokines. The objective of this study was to examine the increase in the anti-inflammatory effect of Gentiana scabra Bunge (GSB), due to bioconversion with the Aspergillus kawachii crude enzyme, via inhibition of the NF-κB signaling and MAP kinase pathways in RAW 264.7 cells. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 in RAW 264.7 cells treated with the GSB ethyl acetate fraction bioconverted with A. kawachii crude enzyme (GE-BA), was dramatically suppressed as compared to GSB ethyl acetate fraction non-bioconverted with the A. kawachii crude enzyme (GE-UA). The phosphorylation of p38, extracellular signalregulated kinases, and inhibitory κB in RAW 264.7 cells treated with GE-BA was further suppressed, as compared to exposure to GE-UA. Moreover, the mRNA expression of interleukin 6, interleukin 1-beta, and tumor necrosis factor-α was further suppressed by GE-BA, compared to GE-UA. Similarly, antioxidant activities, such as 2,2-diphenyl-1-picrylhydrazyl hydrate and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) radical scavenging activity, of GE-BA were further increased compared to GE-UA. These observations demonstrate that the anti-oxidant and anti-inflammatory activities of GSB ethyl acetate fraction increases as a result from bioconversion with the A. kawachii crude enzyme.

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“…Formalin‐fixed paraffin‐embedded left ventricular sections were used for histopathological analysis. Hematoxylin and eosin (H&E) staining was performed to identify the changes in cardiac architecture, and Masson‐trichrome (M‐T) staining was performed to estimate the cardiac fibrosis.…”

Section: Methodsmentioning

confidence: 99%

Comparative evaluation of torasemide and spironolactone on adverse cardiac remodeling in a rat model of dilated cardiomyopathy

Arumugam

Sreedhar

Karuppagounder

et al. 2017

Cardiovascular Therapeutics

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Naringenin ameliorates daunorubicin induced nephrotoxicity by mitigating AT1R, ERK1/2-NFκB p65 mediated inflammation

Cited by 47 publications

References 40 publications

Naringenin Inhibits Superoxide Anion-Induced Inflammatory Pain: Role of Oxidative Stress, Cytokines, Nrf-2 and the NO−cGMP−PKG−KATPChannel Signaling Pathway

Naringenin Inhibits Superoxide Anion-Induced Inflammatory Pain: Role of Oxidative Stress, Cytokines, Nrf-2 and the NO−cGMP−PKG−KATPChannel Signaling Pathway

Bioconversion ofGentiana scabraBunge increases the anti-inflammatory effect in RAW 264.7 cells via MAP kinases and NF-κB pathway

Comparative evaluation of torasemide and spironolactone on adverse cardiac remodeling in a rat model of dilated cardiomyopathy

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