Epigallocatechin-3-gallate attenuates cadmium-induced chronic renal injury and fibrosis

Chen, Jinglou; Du, Lifen; Li, Jingjing; Song, Ho-Young

doi:10.1016/j.fct.2016.07.030

Cited by 64 publications

(32 citation statements)

References 31 publications

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“…When the balance of oxidation-antioxidation is destroyed, the oxidative stress promoted tissue deficits emerge. MDA and NO are suggested to be the markers of Cd-induced oxidative stress [22]. MDA indicates the degree of cell membranes damages induced by organic lipid peroxidation [23].…”

Section: Discussionmentioning

confidence: 99%

Potential Ameliorative Effects of Qing Ye Dan Against Cadmium Induced Prostatic Deficits via Regulating Nrf-2/HO-1 and TGF-β1/Smad Pathways

Lei

Chen

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cadmium (Cd) is an environmental pollutant with reproductive toxicity. Swertia mileensis is used in Chinese medicine for the treatment of prostatic deficits and named as Qing Ye Dan (QYD). This study was undertaken to investigate the potential protective effects of QYD against Cd-induced prostatic deficits. Method: Rat model of prostatic deficits was induced by 0.2 mg/kg/d CdCl₂ subcutaneous injection for 15 days. The prostatic oxidative stress was evaluated by detecting the levels of malondialdehyde, nitric oxide, reduced/ oxidized glutathione, total sulfhydryl groups and enzymatic antioxidant status. The prostatic inflammation was estimated by testing the levels of pro-inflammatory cytokines. The levels of epithelial-mesenchymal transition (EMT) markers E-cadherin, fibronectin, vimentin and α-smooth muscle actin were measured by qPCR analysis. Additionally, the prostatic expressions of transforming growth factor-β1 (TGF-β1), type I TGF-β receptor (TGF-βRI), Smad2, phosphorylation-Smad2 (p-Smad2), Smad3, p-Smad3, Smad7, nuclear related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), B-cell CLL/lymphoma (Bcl)-2 and Bcl-2-associated X protein (Bax) were measured by western blot assay. Results: It was found that QYD ameliorated the Cd-induced prostatic oxidative stress and inflammation, attenuated prostatic EMT, inhibited the TGF-β1/Smad pathway, increased Bcl-2/Bax ratio and enhanced the activity of Nrf-2/HO-1 pathway. Conclusion: These results showed that QYD could ameliorate Cd-induced prostatic deficits via modulating Nrf-2/HO-1 and TGF-β1/Smad pathways.

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Section: Discussionmentioning

confidence: 99%

Potential Ameliorative Effects of Qing Ye Dan Against Cadmium Induced Prostatic Deficits via Regulating Nrf-2/HO-1 and TGF-β1/Smad Pathways

Lei

Chen

et al. 2017

Cell Physiol Biochem

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“…In literature, the beneficial action of dietary and plantderived antioxidants on toxicity of some of the heavy metals has been reported. For example, flavonoids such as epigallocatechin gallate and curcumin have been shown to possess protective activity against cadmium-induced nephrotoxicity in rats [5,6]. Catechin hydrate has been found to reduce cytotoxic and genotoxic effects of cadmium in human peripheral blood lymphocytes [7].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Dietary Antioxidants against Vanadium-Induced Toxicity: A Review

Zwolak

2020

Oxidative Medicine and Cellular Longevity

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Vanadium (V) in its inorganic forms is a toxic metal and a potent environmental and occupational pollutant and has been reported to induce toxic effects in animals and people. In vivo and in vitro data show that high levels of reactive oxygen species are often implicated in vanadium deleterious effects. Since many dietary (exogenous) antioxidants are known to upregulate the intrinsic antioxidant system and ameliorate oxidative stress-related disorders, this review evaluates their effectiveness in the treatment of vanadium-induced toxicity. Collected data, mostly from animal studies, suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity. These findings show potential preventive effects of dietary antioxidants on vanadium-induced oxidative stress, DNA damage, neurotoxicity, testicular toxicity, and kidney damage. The relevant mechanistic insights of these events are discussed. In summary, the results of studies on the role of dietary antioxidants in vanadium toxicology appear encouraging enough to merit further investigations.

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“…The most abundant polyphenol in green tea, (-)-epigallocatechin-3-gallate (EGCG) (Fig. 1), is a potent antioxidant and exhibits extensive pharmacological activity including antioxidative, anti-inflammatory, anti-cancer and immunomodulatory properties [11-14]. The antioxidative activity of EGCG plays a crucial role against the above mentioned disease.…”

Section: Introductionmentioning

confidence: 99%

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

Yu¹,

Pei

Huang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Exposure to arsenic in individuals has been found to be associated with various health-related problems including skin lesions, cancer, and cardiovascular and immunological disorders. (-)-Epigallocatechin-3-gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, anti-apoptotic and anti-inflammatory activity in vivo and in vitro. Thus, the present study was conducted to investigate the protective effects of EGCG against arsenic-induced inflammation and immunotoxicity in mice. Methods: Serum IL-1β, IL-6 and TNF-α were determined by ELISA, tissue catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide and caspase 3 by commercial kits, mitochondrial membrane potential with Rh 123, mitochondrial ROS with 2’,7’-dichlorofluorescin diacetate (DCFH-DA), apoptotic and necrotic cells and T-cell phenotyping with Flow cytometry analysis. Results: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis. Arsenic exposure increased the relative frequency of the CD8+(Tc) cell subpopulation (from 2.8 to 18.9%) and decreased the frequency of CD4+(Th) cells (from 5.2 to 2.7%). Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%). All of these effects induced by NaAsO₂ were attenuated by EGCG. Conclusions: The present in vitro findings indicate that EGCG attenuates not only NaAsO₂-induced immunosuppression but also inflammation and apoptosis.

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Epigallocatechin-3-gallate attenuates cadmium-induced chronic renal injury and fibrosis

Cited by 64 publications

References 31 publications

Potential Ameliorative Effects of Qing Ye Dan Against Cadmium Induced Prostatic Deficits via Regulating Nrf-2/HO-1 and TGF-β1/Smad Pathways

Potential Ameliorative Effects of Qing Ye Dan Against Cadmium Induced Prostatic Deficits via Regulating Nrf-2/HO-1 and TGF-β1/Smad Pathways

Protective Effects of Dietary Antioxidants against Vanadium-Induced Toxicity: A Review

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

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