Epigallocatechin gallate supplementation protects against renal injury induced by fluoride intoxication in rats: Role of Nrf2/HO-1 signaling

Thangapandiyan, S.; Miltonprabu, Selvaraj

doi:10.1016/j.toxrep.2014.01.002

Cited by 59 publications

(41 citation statements)

References 55 publications

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“…Further, the dominant hydrogen-donating activity of EGCG activates the Nrf2 proteins and increase the phase II antioxidants, thereby preventing the Fl-induced generation of ROS/RNS in the rat brain. Moreover, EGCG has been proved to be a potent antioxidant which inhibited the Fl-mediated Keap 1 proteins and DNA damage; lipid peroxidation in the brain, liver, and kidney of rats; and increased the activity of antioxidant enzymes, such as glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT) in rats (Kumar & Kumar, 2009;Thangapandiyan & Miltonprabu, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…The central nervous system had vulnerability to free radical damage due to elevated oxidative metabolic rate and enriched content of unsaturated lipids, as well as its eminent rate of free radical generation derived from neurotransmitters metabolism, and poor radical scavenging mechanisms (Chong, Li, & Maiese, 2005). The oxidative stress-induced free radical damage has been observed in soft tissues such as the liver, kidney, brain, and testes where animals exposed to Fl Thangapandiyan & Miltonprabu, 2014;Nabavi et al, 2012;and Shanthakumari, Srinivasalu, & Subramanian, 2004). Fl exposure decreases the intracellular glutathione levels and can inhibit the activity of several antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase, and catalase (Chlubek & Poland, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…Among them, epigallocatechin gallate (EGCG) (Fig. 1) is one of the versatile polyphenol known for its powerful antioxidant property, protecting cells against freeradical DNA damage, inhibition of lipid peroxidation and protein oxidation (Thangapandiyan & Miltonprabu, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Taking in to account, the previous studies demonstrated that the polyphenols from green tea, especially EGCG, significantly improved the quality of wound healing and remarkably suppressed the hepatic, kidney, and pulmonary toxicity (Thangapandiyan & Miltonprabu, 2014;Thangapandiyan & Miltonprabu, 2014;Thangapandiyan, Miltonprabu, & Senthilraja, 2016). However, there is a paucity of data available on the neuroprotective action of EGCG against Fl-induced hippocampal neurotoxicity in rats.…”

Section: Introductionmentioning

confidence: 99%

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A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Thangapandiyan

Abdulla

Yakulasamy

et al. 2018

JoBAZ

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Background: Fluoride (Fl) exposure engenders neurodegeneration and induces oxidative stress in the brain. Therefore, the mechanism of Fl-induced neurotoxic effects needs to be determined. The aim of this study was to investigate the neuroprotective effects of EGCG (40 mg/kg) on Fl (25 mg/kg/bw)-induced oxidative stress mediated neurotoxicity with special emphasis on the hippocampus (4 weeks).Results: Fl-intoxicated rat shows an increased Fl concentration along with the decreased neurotransmitter (AChE, NP, DA and 5-HT) activity in the brain. The oxidative stress markers (ROS, TBARS, NO, and PC) was significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and nonenzymatic antioxidants (GSH, TSH, and Vit.C) in the rat hippocampus. Moreover, results showed that increases in intrinsic and extrinsic apoptotic pathway leading to DNA damage and cell death were also proved by the immunohistochemical, histological, and ultra-structural studies in the Fl-treated rat hippocampus. In this context, pre-administration of EGCG significantly improved the oxidative stress, biochemical changes, cellular apoptotic and histological alternations by Fl in the hippocampus of rats. Conclusions: These results confirmed the EGCG supplementation might attenuate the Fl-induced neurotoxicity via Nrf2/Keap1 signaling pathway in the rat hippocampus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Thangapandiyan

Abdulla

Yakulasamy

et al. 2018

JoBAZ

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“…It has been documented that these compounds can modulate antioxidant/detoxifying enzymes via activation of nuclear factor erythroid-2 related factor 2 (Nrf2) (Itoh et al 1997;Zhang 2006;Fraga & Oteiza 2011;Thangapandiyan & Miltonprabu 2014) leading to an enhancing of the excretion of xenobiotics, a reduction in the formation of free radicals and, consequently, a reduction in oxidative damage. In this regard, Yao et al (2007) demonstrated that quercetin attenuates ethanolinduced oxidative stress in human hepatocytes through induction Figure 11.…”

Section: Discussionmentioning

confidence: 99%

Eugenia dysentericaDC. (Myrtaceae) exerts chemopreventive effects against hexavalent chromium-induced damagein vitroandin vivo

Ávila

Alvarenga

Ávila

et al. 2016

Pharmaceutical Biology

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Context: Eugenia dysenterica DC. (Myrtaceae) has been widely used in the folk medicine and it presents phytochemicals constituents associated to antioxidant properties. Objective: The objective of this study was to investigate the protective effects of E. dysenterica leaf hydroalcoholic extract (EDE) in vitro and in vivo using AMJ2-C11 cells and Swiss mice exposed to hexavalent chromium [Cr(VI)], respectively. Materials and methods: AMJ2-C11 cells were pretreated with EDE and exposed to Cr(VI) to evaluate cytotoxicity and the pathways involved in the chemopreventive effects of the extract. Mice were daily pretreated with EDE and then exposed to Cr(VI). Survival analysis, histopathological examination and determination of Cr levels in biological tissues were carried out. Results: In vitro studies showed that pretreatment of the AMJ2-C11 cells with EDE protected against the cytotoxicity and oxidative stress induced by Cr(VI). Consequently, the pretreatment with EDE reduced reactive oxygen species and apoptosis triggered by Cr(VI), probably by a marked antioxidant and chelating activities demonstrated by EDE. Regarding in vivo studies, pretreatment for 10 days with EDE increased survival of the mice exposed to Cr(VI). In addition, EDE prevented liver and kidney pathological damages, in parallel with reduction in chromium levels found in these organs and plasma. EDE also showed a marked antioxidant potential associated with the presence of polyphenols, especially flavonoids and tannins, as confirmed by HPLC-PDA. Conclusion: The study showed that EDE protects against Cr(VI)-induced damage in vitro and in vivo supporting further studies for the development of therapeutic products applied to prevent the damage induced by toxic metals, especially Cr(VI).

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Recent Advances of Natural Polyphenols Activators for Keap1‐Nrf2 Signaling Pathway

Zhou

Jiang

et al. 2019

Chemistry & Biodiversity

135

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The Keap1‐Nrf2/ARE signaling pathway is an important defense system against exogenous and endogenous oxidative stress injury. The dysregulation of the signaling pathway is associated with many diseases, such as cancer, diabetes, and respiratory diseases. Over the years, a wide range of natural products has provided sufficient resources for the discovery of potential therapeutic drugs. Among them, polyphenols possess Nrf2 activation, not only inhibit the production of ROS, inhibit Keap1‐Nrf2 protein–protein interaction, but also degrade Keap1 and regulate the Nrf2 related pathway. In fact, with the continuous improvement of natural polyphenols separation and purification technology and further studies on the Keap1‐Nrf2 molecular mechanism, more and more natural polyphenols monomer components of Nrf2 activators have been gradually discovered. In this view, we summarize the research status of natural polyphenols that have been found with apparent Nrf2 activation and their action modes. On the whole, this review may guide the design of novel Keap1‐Nrf2 activator.

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Epigallocatechin gallate supplementation protects against renal injury induced by fluoride intoxication in rats: Role of Nrf2/HO-1 signaling

Abstract: Graphical abstract

Cited by 59 publications

References 55 publications

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Eugenia dysentericaDC. (Myrtaceae) exerts chemopreventive effects against hexavalent chromium-induced damagein vitroandin vivo

Recent Advances of Natural Polyphenols Activators for Keap1‐Nrf2 Signaling Pathway

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