Epigallocatechin-3-gallate activates Nrf2/HO-1 signaling pathway in cisplatin-induced nephrotoxicity in rats

Şahin, Kazım; Tuzcu, Mehmet; Gençoğlu, Hasan; Doğukan, Ayhan; Timurkan, Mustafa; Şahin, Nurhan; Aslan, Abdullah Nabi; Küçük, Ömer

doi:10.1016/j.lfs.2010.06.014

Cited by 189 publications

(129 citation statements)

References 43 publications

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“…In contrast natural phytochemical Nrf2 activators such as sulforaphane, epigallocatechin-3-gallate, and curcumin, improve nephropathy in animal models of acute or chronic kidney diseases of diverse etiologies [19][20][21][22][23]. Together these observations support the role of Nrf2 deficiency in the pathogenesis of oxidative stress, inflammation, and progression of kidney disease.…”

Section: Introductionmentioning

confidence: 64%

“…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%

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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: Introductionmentioning

confidence: 64%

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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“…Moreover, renal antioxidant defense was significantly improved in EGCG-treated animals in contrast with the depletion registered in CP-controls. 42 The association between antioxidant and antiinflammatory activities of EGCG and its protective role against CP-induced nephrotoxicity has been shown by El-Mowafy and coworkers in mice bearing Ehrlich ascites carcinoma (EAC). 43 This study showed that EGCG administered in combination with CP [ Serum urea and creatinine.…”

Section: Nephrotoxicitymentioning

confidence: 97%

Green tea polyphenol epigallocatechin-3-gallate (EGCG) as adjuvant in cancer therapy

et al. 2013

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s u m m a r yBackground & aims: Green tea catechins, especially epigallocatechin-3-gallate (EGCG), have been associated with cancer prevention and treatment. This has resulted in an increased number of studies evaluating the effects derived from the use of this compound in combination with chemo/radiotherapy. This review aims at compiling latest literature on this subject. Methods: Keywords including EGCG, cancer, chemotherapy, radiotherapy and side effects, were searched using PubMed and ScienceDirect databases to identify, analyze, and summarize the research literature on this topic. Most of the studies on this subject up to date are preclinical. Relevance of the findings, impact factor, and date of publication were critical parameters for the studies to be included in the review. Results: Additive and synergistic effects of EGCG when combined with conventional cancer therapies have been proposed, and its anti-inflammatory and antioxidant activities have been related to amelioration of cancer therapy side effects. However, antagonistic interactions with certain anticancer drugs might limit its clinical use. Conclusions: The use of EGCG could enhance the effect of conventional cancer therapies through additive or synergistic effects as well as through amelioration of deleterious side effects. Further research, especially at the clinical level, is needed to ascertain the potential role of EGCG as adjuvant in cancer therapy.

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“…EGCG, the most abundant polyphenol, has versatile preventive effects toward several chronic diseases including cancer, inflammation, heart disease, diabetes, and neurodegenerative diseases (Chung et al 2001;Li et al 2010;Hosakawa et al 2010;Suganuma et al 1998;Paquay et al 2000;Cai and Lin 2009;Rezai-Zadeh et al 2008). In addition, GTPs are strong antioxidants against ROS as well as inducers of several antioxidant proteins [HO-1, NAD(P) H:quinone oxidoreductase 1 (NQO1), glutathione S-transferase pi (GSTP1), manganese superoxide dismutase] (Sahin et al 2010;Ogborne et al 2008;Na et al 2008).…”

mentioning

confidence: 99%

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

Inoue

Akiyama

Maeda‐Yamamoto

et al. 2011

Cell Stress and Chaperones

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Previously, we reported that oral feeding of 1% green tea polyphenols (GTPs) aggravated the dextran sulfate sodium (DSS)-induced colitis in mice. In the present study, we assessed the toxicity of 1% GTPs in several organs from normal and DSS-exposed mice. Sixty-two male ICR mice were initially divided into four groups. Nontreated group (group 1, n=15) was given standard diet and water, GTPs (group 2, n=15) received 1% GTPs in diet and water, DSS (group 3, n=15) received diet and 5% DSS in water, and GTPs + DSS group (group 4, n=17) received 1% GTPs in diet and 5% DSS in water. We found that group 4 significantly increased (P<0.05) kidney weight, the levels of serum creatinine and thiobarbituric acid-reactive substances in both kidney and liver, as compared with those in group 3. The mRNA expression levels of antioxidant enzymes and heat-shock proteins (HSPs) in group 4 were lower than those of group 3. For instance, heme oxygenase-1 (HO-1), HSP27, and 90 mRNA in the kidney of group 4 were dramatically down-regulated as compared with those of group 3. Furthermore, 1% GTPs diet decreased the expression of HO-1, NAD(P)H:quinone oxidoreductase 1 (NQO1) and HSP90 in kidney and liver of non-treated mice. Taken together, our results indicate that high-dose GTPs diet disrupts kidney functions through the reduction of antioxidant enzymes and heat-shock protein expressions in not only colitis but also non-treated ICR mice.

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Epigallocatechin-3-gallate activates Nrf2/HO-1 signaling pathway in cisplatin-induced nephrotoxicity in rats

Cited by 189 publications

References 43 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

Green tea polyphenol epigallocatechin-3-gallate (EGCG) as adjuvant in cancer therapy

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

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