Epigallocatechin gallate, an active ingredient from green tea, attenuates damaging influences to the retina caused by ischemia/reperfusion

Zhang, Bo; Safa, Rukhsana; Rusciano, Dario; Osborne, Neville N.

doi:10.1016/j.brainres.2007.05.029

Cited by 84 publications

(61 citation statements)

References 79 publications

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“…Activation of these pathways confers protection by up-regulating expression of antioxidant enzymes, detoxifying compounds, protein chaperones, and trophic factors. In fact these phytochemicals have been shown to prevent or ameliorate a variety of diseases including cardiovascular disease [42,43], neurodegenerative disorders [44][45][46][47][48][49], and acute and chronic kidney disease [19][20][21][22][23]. In contrast, excessive or unrestrained activity of Nrf2 system has been shown to have adverse consequences.…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Vaziri¹,

Liu²,

Farzaneh³

et al. 2015

Free Radical Biology and Medicine

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Oxidative stress and inflammation play a central role in progression and complications of CKD and are, in part, due to impairment of the Nrf2 system which regulates expression of antioxidant and detoxifying molecules. Natural Nrf2 inducing phytochemicals have been shown to ameliorate kidney disease in experimental animals. However due to adverse outcomes clinical trial of synthetic Nrf2 activator, bardoxolone methyl (BARD), in CKD patients was terminated. BARD activates Nrf2 via 2 covalent modification of reactive cysteine residues in Nrf2 repressor molecule, Keap-1. In addition to Nrf2, Keap1 suppresses IKKB, the positive regulator of NF k B. Treatment with BARD analog, dh404, at 5-20 mg/kg/day in diabetic obese Zucker rats exacerbates whereas its use at 2 mg/kg/day in 5/6 nephrectomized rats attenuates CKD progression. We, therefore, hypothesized that deleterious effects of high dose BARD are mediated by activation of NF k B.CKD (5/6 nephrectomized) rats were randomized to receive dh404 (2 or 10mg/kg/day) or vehicle for 12 weeks. Vehicle-treated group exhibited glomerulosclerosis, interstitial fibrosis and inflammation, activation of NF k B, upregulation of oxidative, inflammatory and fibrotic pathways, and suppression of Nrf2 activity and its key target gene products. Treatment with low dose dh404 restored Nrf2 activity and expression of its target genes, attenuated activation of NF k B and fibrotic pathways, and reduced glomerulosclerosis, interstitial fibrosis and inflammation. In contrast treatment with high dh404 dosage intensified proteinuria, renal dysfunction and histological abnormalities, amplified up-regulations of NF k B and fibrotic pathways, and suppression of Nrf2 system. Thus therapy with BARD analogs exerts a dose-dependent dimorphic impact on CKD progression.

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Section: Discussionmentioning

confidence: 99%

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Vaziri¹,

Liu²,

Farzaneh³

et al. 2015

Free Radical Biology and Medicine

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“…In RGCs, glutamate toxicity is primarily mediated by NDMA receptors (Sun et al 2001;Calzada et al 2002;Holmgaard et al 2008;Teuchner et al Neuroprotective effect of epigallocatechin-3-gallate against N-methyl-d-aspartateinduced excitotoxicity in the adult rat retina (Sun et al 2001;Ju et al 2009). Epigallocatechin-3-gallate (EGCG) is a powerful antioxidant exhibiting multifunctional properties including anti-inflammatory and antiapoptotic effects and has shown neuroprotective effects in vivo and in vitro studies (Sutherland et al 2006;Zhang et al 2007Zhang et al , 2008Peng et al 2008;Osborne 2009;Xie et al 2010). It has been reported that EGCG protected HT-22 cells (mouse hippocampal cell line) and PC12 cells (pheochromocytoma cell line from the rat adrenal medulla) against glutamate neurotoxicity (Lee et al 2004a,b;Fu & Koo 2006) and that it reduced cell death rate after exposure to the glutamate receptor against NMDA, AMPA or kainite in primary hippocampal cell cultures (Lee et al 2004b).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of epigallocatechin‐3‐gallate against N‐methyl‐D‐aspartate‐induced excitotoxicity in the adult rat retina

Chen

Jiang

Shen

et al. 2012

Acta Ophthalmologica

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ABSTRACT.Purpose: Epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, has been suggested to reduce glutamate excitotoxicity. We therefore investigated the potentially protective effects of EGCG against N-methyl-d-aspartate (NMDA)-induced excitotoxicity in the retina. Methods: Female Wistar rats (n = 171) were divided into a normal control group (n = 9); saline control group with intravitreal saline injections (n = 54); NMDA control group with an intravitreal NMDA injection and intraperitoneal saline injections (n = 54); and NMDA study group (n = 54) receiving an intravitreal NMDA injection plus intraperitoneal EGCG (25 mg ⁄ kg) injections. Starting at 2 days prior to the intravitreal NMDA injection, the intraperitoneal injections were performed daily for the whole study period. At 12 hr, 1, 2, 3 days, 1 and 2 weeks after the intravitreal NMDA injection, the animals were killed. We counted the neurons in the retinal ganglion cell layer (GCL) on histological sections, measured the thickness of Thy-1 immunoreactivity and assessed the expression of Thy-1 mRNA by real-time polymerase chain reaction. Results: At all time-points, GCL cell density, thickness of Thy-1 immunoreactivity and expression of Thy-1 mRNA were significantly (all p < 0.05) lower in the NMDA control group than in the NMDA study group, in which the parameters were significantly (all p < 0.05) lower than in the saline control group and the normal control group. In both groups with an intravitreal NMDA injection, GCL cell density, thickness of Thy-1 immunoreactivity and expression of Thy-1 mRNA decreased significantly with increasing follow-up time. Conclusions: Intraperitoneal application of EGCG resulted in a significantly less marked NMDA-associated loss of retinal ganglion cells.

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“…Decreased mRNA levels of ganglion cell specific markers Thy-1 and NF-L, and opsin (photoreceptor marker) in retina were reversed by EGCG on the one hand and increased mRNA levels of caspase-3, caspase-8, and glial fibrillary acidic protein (directly related to retinal degeneration) were reduced on the other (39) ( Table 5). Similarly, decreased protein levels of NF-L and rhodopsin kinase (photoreceptor marker) in retina were increased whereas increased protein levels of caspase-3 and glial fibrillary acidic protein were attenuated by EGCG (39). In the optic nerve, where many ganglion cell axons are present, the reductions in NF-L and tubulin proteins, proteins expressed by ganglion cells, caused by I/R were also counteracted by EGCG (39).…”

Section: Retinamentioning

confidence: 96%

“…Regarding in vivo experiments, EGCG was able to inhibit the alterations seen in a and b-waves (informative for the photoreceptors and the ON-bipolar/Müller cells, respectively) measured by the electroretinogram (39). Negative effects of I/R on Thy-1 and ChAT immunoreactivities, associated with ganglion cells and a sub-set of amacrine cells in inner retina, were prevented by EGCG as well (39). Decreased mRNA levels of ganglion cell specific markers Thy-1 and NF-L, and opsin (photoreceptor marker) in retina were reversed by EGCG on the one hand and increased mRNA levels of caspase-3, caspase-8, and glial fibrillary acidic protein (directly related to retinal degeneration) were reduced on the other (39) ( Table 5).…”

Section: Retinamentioning

confidence: 98%

“…Similarly, decreased protein levels of NF-L and rhodopsin kinase (photoreceptor marker) in retina were increased whereas increased protein levels of caspase-3 and glial fibrillary acidic protein were attenuated by EGCG (39). In the optic nerve, where many ganglion cell axons are present, the reductions in NF-L and tubulin proteins, proteins expressed by ganglion cells, caused by I/R were also counteracted by EGCG (39). Same group showed, in another in vitro study, that EGCG is able to prevent lightinduced cell death, apoptosis, reactive oxygen species production, and loss of mitochondrial dehydrogenase activity in retina ganglion cells (40) (Table 5).…”

Section: Retinamentioning

confidence: 99%

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Deney hayvanlarındaki iskemi-reperfüzyon hasarı modellerinde yeşil çayın etkileri

Ergün¹

2017

Kahramanmaraş Sütçü İmam Üniversitesi Tıp Fakültesi Dergisi

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Özetİskemi-reperfüzyon hasarı beyin, çizgili kas, kalp, bağırsak, karaciğer, böbrekler, retina, pankreas ve testis gibi farklı dokuları kapsayan çeşit-li birçok klinik durumda ortaya çıkmaktadır. Her ne kadar oksidatif stresin iskemi-reperfüzyon hasarının etiyolojisinde merkezi bir rol oynadığı gösterişmiş olsa da, inflamasyon, lökosit infiltrasyonu ve apoptozis gibi birçok mekanizma da dahil edilmiştir. İskemi-reperfüzyon hasarını azaltmak için bugüne kadar çeşitli maddeler test edilmiştir. Ancak, hiçbiri bu endikasyonda kullanılmak üzere medikal ürün olarak henüz geliştirilmemiştir. Bu bağlamda, yeşil çay içerikler-inin farklı formdaki hayvan iskemi-reperfüzyon hasarı modellerinde faydalı etkiler gösterdikleri bulunmuştur. Bu derlemede, yeşil çay içeriklerinin hayvan iskemi-reperfüzyon hasarı modelleri üzerindeki etkileri tarihsel ve dokuya spesifik bir şekilde tartışılmıştır.Anahtar Kelimeler: Epigallokateşin gallat; yeşil çay; iskemi-reperfüzyon hasarı AbstractIschemia-reperfusion injury appears in various types of clinical conditions involving different tissues such as brain, skeletal muscle, heart, gut, liver, kidney, retina, pancreas and testis. Although oxidative stress has been shown to have a pivotal role in the aetiology of ischemia-reperfusion injury, several mechanisms including inflammation, leukocyte infiltration and apoptosis have been included as well. In an attempt to reduce ischemia-reperfusion injury, various substances have been tested so far. However, none of them have evolved as a medicinal product to be used in these indications yet. In this context, green tea contents have been shown to possess favourable effects in distinct forms of animal models relating to ischemia-reperfusion injury. In this review, the effects of green tea contents on ischemia-reperfusion injury models of animals have been discussed in a historical and tissue-specific manner.

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Epigallocatechin gallate, an active ingredient from green tea, attenuates damaging influences to the retina caused by ischemia/reperfusion

Cited by 84 publications

References 79 publications

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Neuroprotective effect of epigallocatechin‐3‐gallate against N‐methyl‐D‐aspartate‐induced excitotoxicity in the adult rat retina

Deney hayvanlarındaki iskemi-reperfüzyon hasarı modellerinde yeşil çayın etkileri

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