Protective Effect of Combined Caffeic Acid Phenethyl Ester and Bevacizumab Against Hydrogen Peroxide-Induced Oxidative Stress in Human RPE Cells

Dinç, Erdem; Ayaz, Lokman; Kurt, Akif Hakan

doi:10.1080/02713683.2017.1368085

Cited by 21 publications

(16 citation statements)

References 33 publications

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“…40,41 This phenomenon was normalized by N-acetylcysteine (NAC) ( Figure 1A). 40,41 This phenomenon was normalized by N-acetylcysteine (NAC) ( Figure 1A).…”

Section: Oxidative Stress Down-regulates Mir-205-5p Expressionmentioning

confidence: 98%

“…As previously observed, ARPE-19 cells resulted in a significant ROS production after 600 µM H 2 O 2 exposure. 40,41 This phenomenon was normalized by N-acetylcysteine (NAC) ( Figure 1A). Significantly reduced miR-205-5p levels were observed in ARPE-19 cells after H 2 O 2 exposure compared with control cells ( Figure 1B).…”

Section: Oxidative Stress Down-regulates Mir-205-5p Expressionmentioning

confidence: 98%

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Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Oltra

Vidal-Gil

Maisto³

et al. 2019

J Cellular Molecular Medi

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miR‐205‐5p is known to be involved in VEGF‐related angiogenesis and seems to regulate associated cell signalling pathways, such as cell migration, proliferation and apoptosis. Therefore, several studies have focused on the potential role of miR‐205‐5p as an anti‐angiogenic factor. Vascular proliferation is observed in diabetic retinopathy and the ‘wet’ form of age‐related macular degeneration. Today, the most common treatments against these eye‐related diseases are anti‐VEGF therapies. In addition, both AMD and DR are typically associated with oxidative stress; hence, the use of antioxidant agents is accepted as a co‐adjuvant therapy for these patients. According to previous data, ARPE‐19 cells release pro‐angiogenic factors when exposed to oxidative insult, leading to angiogenesis. Matching these data, results reported here, indicate that miR‐205‐5p is modulated by oxidative stress and regulates VEGFA‐angiogenesis. Hence, miR‐205‐5p is proposed as a candidate against eye‐related proliferative diseases.

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“…40,41 This phenomenon was normalized by N-acetylcysteine (NAC) ( Figure 1A). 40,41 This phenomenon was normalized by N-acetylcysteine (NAC) ( Figure 1A).…”

Section: Oxidative Stress Down-regulates Mir-205-5p Expressionmentioning

confidence: 98%

Section: Oxidative Stress Down-regulates Mir-205-5p Expressionmentioning

confidence: 98%

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Oltra

Vidal-Gil

Maisto³

et al. 2019

J Cellular Molecular Medi

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“…Genomic instability is generally compensated by DNA repair systems in a healthy individual. However, it has been reported that diminished antioxidant defense and DNA repair systems, which leads damaged genome and subsequent cell loss, contribute pathogenesis of many diseases (9,20,21). In the current study, alkali comet assay was used, which has been shown to be reliable, sensitive and cost effective method for detecting DNA strand breaks, alkali labile sites in DNA and incomplete excision repair sites at the level of a single cell.…”

Section: Resultsmentioning

confidence: 91%

“…Comparison of total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) values between the control and AMD groups Discussion RPE is exposed to excessive amounts of ROS due to chronic light exposure and high oxygen consumption. However, various antioxidant enzymes and defense mechanisms protect the RPE against oxidative damage (9,20,21). On the other hand, AMD has been suggested to be related with oxidative stress, as in many ocular diseases, whereas it is also wellknown that AMD is a multifactorial disease and underlying mechanisms are still unclear (1)(2)(3)(4)(5).…”

Section: Resultsmentioning

confidence: 99%

Systemic Oxidant and Genotoxic Background in Exudative Age-Related Macular Degeneration

Toprak

Yaylalı

et al. 2019

Süleyman Demirel Üniversitesi Sağlık Bilimleri Dergisi

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Bu çalışmanın amacı eksudatif tip yaşa bağlı makula dejenerasyonu (YBMD) tanılı hastalarda sistemik oksidatif stres ve genotoksisite (DNA hasarı) düzeylerini belirleyerek bu faktörlerin ileri evre yaş tip YBMD gelişimindeki olası rolünü araştırmaktır. Materyal-Metot: Çalışmaya eksudatif YBMD tanılı 26 hasta (68,9±1,9 yaş) ve 26 yaş ve cinsiyet uyumlu (64,8±2,2 yaş) sağlıklı kontrol grubu (p=0,268, p=0,258) dahil edildi. Serum total antioksidan durumu (TAS) ve total oksidan durumu (TOS) ticari bir kit kullanılarak ölçüldü. Oksidatif stres indeksi (OSİ) hesaplandı. DNA hasarı, venöz tam kandan lenfosit izolasyonunu takiben Comet (kuyruklu yıldız) analizi kullanılarak değerlendirildi. Kuyruk uzunluğu ve kuyruk momenti dahil olmak üzere parametreler, DNA hasarının kantitatif analizi için değerlendirildi. Bulgular: YBMD grubunda kontrol grubuna göre daha düşük TAS ve daha yüksek OSİ değerleri mevcut iken, TOS değerleri iki grup arasında farklılık göstermedi (p=0,006, p=0,039, p=0,319, sırasıyla). Ayrıca, YBMD grubunda kuyruk uzunluğu (p<0,0001) ve kuyruk momenti (p=0,005) kontrol grubuna göre anlamlı olarak yüksek bulundu. Sonuç: YBMD patogenezinde birçok faktör rol oynamasına karşın, artmış sistemik oksidatif stres ve DNA hasarı eksudatif YBMD gelişimi konusunda önemli bir risk faktörü olabilir. Ayrıca, bu faktörlerin erken evre YBMD hastalarında da araştırılması yeni önleme tedavilerinin geliştirilmesi bakımından yol gösterici olabilir.

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“…Unfortunately, they do not renew after differentiation ( Ebrahimi et al, 2017 ), inevitably resulting in RPE apoptosis caused by long-term oxidative damage. In severe AMD cases, these apoptotic RPE cells release VEGF, the most significant pro-angiogenic factor, resulting in the activation of CNV and the further development of wet AMD ( Dinc et al, 2017 ). Therefore, it is imperative to inhibit RPE cell apoptosis for abrogating subsequent angiogenesis in AMD.…”

Section: Introductionmentioning

confidence: 99%

Kinsenoside Ameliorates Oxidative Stress-Induced RPE Cell Apoptosis and Inhibits Angiogenesis via Erk/p38/NF-κB/VEGF Signaling

Luo¹,

Gu²,

Zhang³

et al. 2018

Front. Pharmacol.

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The pathological superoxidative condition that retinal pigment epithelium (RPE) cells experience contributed to the advancement of age-related macular degeneration (AMD), which was accompanied by significant neovascularization. Therefore, the discovery of novel pharmacological candidates to ameliorate oxidative damage (H2O2) against RPE cells and inhibit the following angiogenesis simultaneously is urgently needed. Herein, we found that kinsenoside (Kin), an active component derived from Anoectochilus roxburghii, was able to protect RPE cells effectively and attenuate subsequent angiogenesis. In this study, H2O2-induced oxidative injury reduced RPE cell viability and increased cell apoptosis, which was significantly rescued by the treatment with Kin. Compared with H2O2 alone, Kin decreased the levels of Bax and increased the production of Bcl-2 in RPE cells. H2O2-stimulated VEGF up-regulation was inhibited by Kin treatment. Human umbilical vein endothelial cell (HUVEC) neovascularization induced by conditioned medium (CM) from H2O2-stimulated RPE cells was attenuated by treatment with Kin, VEGF antagonist, NF-κB, Erk-MAPK, and p38-MAPK inhibitors. Additionally, H2O2-activated phosphorylated expression of IκBα, p65, Erk, and p38 in RPE cells was inhibited by treatment with Kin. Taken together, Kin protected RPE from apoptosis against oxidative stress while simultaneously decreasing apoptosis-related neovascularization. This could be ascribed to the inhibition of Erk/p38/NF-κB signaling by Kin that contributed to the resulting decreased VEGF expression in H2O2-treated RPE cells.

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Protective Effect of Combined Caffeic Acid Phenethyl Ester and Bevacizumab Against Hydrogen Peroxide-Induced Oxidative Stress in Human RPE Cells

Cited by 21 publications

References 33 publications

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Systemic Oxidant and Genotoxic Background in Exudative Age-Related Macular Degeneration

Kinsenoside Ameliorates Oxidative Stress-Induced RPE Cell Apoptosis and Inhibits Angiogenesis via Erk/p38/NF-κB/VEGF Signaling

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