Epigallocatechin Gallate (EGCG) Prevents H2O2-Induced Oxidative Stress in Primary Rat Retinal Pigment Epithelial Cells

Cia, David; Vergnaud-Gauduchon, Juliette; Jacquemot, Nathalie; Doly, M.

doi:10.3109/02713683.2014.885532

Cited by 30 publications

(28 citation statements)

References 45 publications

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“…These findings are consistent with the results of a previous study (18). H 2 O 2 -mediated apoptosis is a mixed response involving numerous apoptotic pathways, which includes activation of the caspase pathways and dysregulation of the Bcl-2/Bax balance (19,20). caspase-3 is a key regulatory protein in the caspase-dependent apoptotic pathway (21,22), which can be activated by caspase-8/9.…”

Section: Discussionsupporting

confidence: 92%

BMP‑6 protects retinal pigment epithelial cells from oxidative stress‑induced injury by inhibiting the MAPK signaling pathways

et al. 2018

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Worldwide, neovascular age‑related macular degeneration (nAMD) is one of the most common causes of blindness in the elderly. In particular, degeneration of retinal pigment epithelial (RPE) cells represents the main pathological process in the development of nAMD, and oxidative stress serves a major role. The present study aimed to investigate the association between bone morphogenetic protein 6 (BMP‑6) and nAMD. BMP‑6 concentration was significantly reduced in patients with wet nAMD compared with in the control group. Furthermore, the present study investigated the protective effects of BMP‑6 on RPE cells following oxidative stress‑induced injury. Cell Counting Kit‑8 assay and terminal deoxynucleotidyl transferase dUTP nick‑end labeling staining demonstrated that BMP‑6 increased RPE cell viability, which was decreased following treatment with hydrogen peroxide (H2O2), and reduced H2O2‑induced apoptosis. In addition, western blotting revealed that BMP‑6 reversed the decrease in pro‑caspase‑3 levels and the dysregulation of the B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein (Bax) balance caused by H2O2. In addition, alterations in c‑Jun N‑terminal protein kinase (JNK) and p38 mitogen‑activated protein kinase (MAPK) expression were examined, and pretreatment with BMP‑6 was demonstrated to reduce H2O2‑induced activation of JNK and p38 MAPK. Conversely, the effects of BMP‑6 were attenuated by its inhibitor noggin. In conclusion, the present study demonstrated that BMP‑6 may protect RPE cells from oxidative stress injury to a certain extent, which may be associated with alterations in the MAPK signaling pathway. However, the specific mechanism of action underlying this effect requires further investigation. Overall, the present study laid a foundation for exploring novel nAMD treatment methods.

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Section: Discussionsupporting

confidence: 92%

BMP‑6 protects retinal pigment epithelial cells from oxidative stress‑induced injury by inhibiting the MAPK signaling pathways

et al. 2018

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“…Treatment with H 2 O 2 resulted in cell viability loss with an IC50 close to 450 lM (Fig. 1B) as previously reported [29]. Therefore, concentrations of 50 lM atRAL and 450 lM H 2 O 2 were initially used as the working concentrations.…”

Section: Cytotoxic Effects Of At Ral and H 2 O 2 On Rpe Cellssupporting

confidence: 70%

Phloroglucinol protects retinal pigment epithelium and photoreceptor against all‐trans‐retinal–induced toxicity and inhibits A2E formation

Cia

Cubizolle

Crauste

et al. 2016

J Cellular Molecular Medi

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Among retinal macular diseases, the juvenile recessive Stargardt disease and the age-related degenerative disease arise from carbonyl and oxidative stresses (COS). Both stresses originate from an accumulation of all-trans-retinal (atRAL) and are involved in bisretinoid formation by condensation of atRAL with phosphatidylethanolamine (carbonyl stress) in the photoreceptor and its transformation into lipofuscin bisretinoids (oxidative stress) in the retinal pigment epithelium (RPE). As atRAL and bisretinoid accumulation contribute to RPE and photoreceptor cell death, our goal is to select powerful chemical inhibitors of COS. Here, we describe that phloroglucinol, a natural phenolic compound having anti-COS properties, protects both rat RPE and mouse photoreceptor primary cultures from atRAL-induced cell death and reduces hydrogen peroxide (H 2 O 2 )-induced damage in RPE in a dose-dependent manner. Mechanistic analyses demonstrate that the protective effect encompasses decrease in atRAL-induced intracellular reactive oxygen species and free atRAL levels. Moreover, we show that phloroglucinol reacts with atRAL to form a chromene adduct which prevents bisretinoid A2E synthesis in vitro. Taken together, these data show that the protective effect of phloroglucinol correlates with its ability to trap atRAL and to prevent its further transformation into deleterious bisretinoids. Phloroglucinol might be a good basis to develop efficient therapeutic derivatives in the treatment of retinal macular diseases.

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“…Previous studies reported that H 2 O 2 can decrease RPE cell viability, which induces AMD progression [21][22][23]. Based on these previous studies, the present study confirmed that H 2 O 2 significantly decreased cell viability and increased intracellular ROS production.…”

Section: Discussionsupporting

confidence: 89%

Exendin-4 Protects Human Retinal Pigment Epithelial Cells from H2O2-Induced Oxidative Damage via Activation of NRF2 Signaling

Cui

Tian

et al. 2019

Ophthalmic Res

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Aims: Oxidative damage plays a vital role in the pathogenesis of age-related macular degeneration (AMD). Exendin-4 (EX4), a glucagon-like peptide-1 receptor agonist, possesses several pharmacological functions, such as anti-inflammatory and antioxidative properties. However, the effects and mechanism of EX4 on oxidative stress in retinal pigment epithelial (RPE) cells induced by hydrogen peroxide (H 2 O 2) remain unclear. The present study aimed to investigate the protective mechanism of EX4 on human RPE cells subjected to oxidative stress. Methods: Human RPE ARPE-19 cells were treated with H 2 O 2 to induce oxidative damage. Cell viability was determined by Cell Counting Kit-8 and lactate dehydrogenase assay. Levels of intracellular reactive oxygen species (ROS), malonyldialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH) were measured using commercial kits. The expression of nuclear factor erythroid 2-related factor-2 (NRF2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO-1) was measured using reverse transcription quantitative polymerase chain reaction assay and western blot, respectively. Results: H 2 O 2 significantly induced oxidative stress to reduce viability of RPE cells and increased intracellular ROS generation. EX4 significantly ameliorated H 2 O 2-induced oxidative damage by reducing intracellular ROS generation, decreasing MDA concentration, and increasing antioxidant enzymes activities (SOD and GSH). In addition, EX4 markedly increased expression of NRF2, HO-1, and NQO-1 and significantly improved protein expression of NRF2 and HO-1 in H 2 O 2-treated ARPE-19 cells, caused by increased nuclear NRF2 protein expression. NRF2 knockdown by targeted siRNA alleviated EX4-mediated HO-1 expression and significantly nullified EX4-mediated RPE cell protection against H 2 O 2. Conclusions: EX4 attenuated oxidative damage induced by H 2 O 2 in ARPE-19 cells through the activation of the NRF2 signaling pathway. The findings suggested that EX4 may be a potential therapeutic agent for the treatment of AMD.

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Epigallocatechin Gallate (EGCG) Prevents H₂O₂-Induced Oxidative Stress in Primary Rat Retinal Pigment Epithelial Cells

Abstract: Our study shows that EGCG pretreatment can protect primary rat RPE cells from H(2)O(2)-induced death. This suggests potential effect of EGCG in the prevention of retinal diseases associated with H(2)O(2)-induced oxidative stress.

Cited by 30 publications

References 45 publications

BMP‑6 protects retinal pigment epithelial cells from oxidative stress‑induced injury by inhibiting the MAPK signaling pathways

BMP‑6 protects retinal pigment epithelial cells from oxidative stress‑induced injury by inhibiting the MAPK signaling pathways

Phloroglucinol protects retinal pigment epithelium and photoreceptor against all‐trans‐retinal–induced toxicity and inhibits A2E formation

Exendin-4 Protects Human Retinal Pigment Epithelial Cells from H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Damage via Activation of NRF2 Signaling

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