Sanguinarine induces apoptosis of human lens epithelial cells by increasing reactive oxygen species via the MAPK signaling pathway

Zhang, Yue; Huang, Wan‐Rong

doi:10.3892/mmr.2019.10087

Cited by 12 publications

(9 citation statements)

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“…AKT signaling pathway is crucial in promoting endothelial cell survival while ERK1/2 and p38 (Tyr182) are vital in proliferation and migration respectively ( Basini et al, 2007c ; Cheng et al, 2017 ). This result was in line with several previous studies that SC demonstrated antiangiogenic and anti-invasive effect ( Cheng et al, 2017 ; Zhang and Huang, 2019 ). However, our result was different from the previous study ( Eun and Koh, 2004 ), which reported that Sanguinarine suppressed VEGF-induced Akt phosphorylation but not ERK 1/2 or PLCr1 phosphorylation.…”

Section: Discussionsupporting

confidence: 93%

“…Vascular Endthelial Growth Factor-Induced Phosphorylation of Anti-Phospho-Protein Kinase B, p38-MAPK and Extracellular Signal-Regulated Kinase 1/2 AKT, p38-MAPK, and ERK1/2 are crucial factors triggered by VEGF to induce the angiogenesis process, including survival, migration and proliferation of endothelial cells (Aiello et al, 1995;Roh et al, 2016;Cheng et al, 2017;Zhang and Huang, 2019). Thus we investigated the effect of SC on VEGF-induced phosphorylation of AKT (p-AKT), p38-MAPK (p-p38-MAPK), and ERK1/2 (p-ERK1/2) using HRMECs ( Figure 7A).…”

Section: Sanguinarine Chloride Suppressedmentioning

confidence: 99%

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The Antiangiogenic Effect of Sanguinarine Chloride on Experimental Choroidal Neovacularization in Mice via Inhibiting Vascular Endothelial Growth Factor

Zhang

Mao

et al. 2021

Front. Pharmacol.

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Background: The purpose of this study is to investigate the antiangiogenic effect of Sanguinarine chloride (SC) on models of age-related macular degeneration (AMD) both in vivo and in vitro.Methods: Choroidal neovascularization (CNV) was conducted by laser photocoagulation in C57BL6/J mice. SC (2.5 μM, 2 μl/eye) was intravitreally injected immediately after laser injury. The control group received an equal amount of PBS. 7 days after laser injury, CNV severity was evaluated using fundus fluorescein angiography, hematoxylin and eosin (H&E) staining, and choroid flat-mount staining. Vascular endothelial growth factor (VEGF) expression in the retina/choroid complex was measured by western blot analysis and ELISA kit. In vitro, human retinal microvascular endothelial cells (HRMECs) were used to investigate the effects of SC on cell tube formation, migration, and cytotoxicity. The expression of VEGF-induced expression of extracellular signal-regulated kinase (ERK)1/2, protein kinase B (AKT), mitogen-activated protein kinases (p38-MAPK) in vitro and laser induced VEGF expression in vivo were also analyzed.Results: SC (≤2.5 μM) was safe both in vitro and in vivo. Intravitreal injection of SC restrained the formation of laser induced CNV in mice and decreased VEGF expression in the laser site of the retina/choroid complex. In vitro, SC inhibited VEGF-induced tube formation and endothelial cell migration by decreasing the phosphorylation of AKT, ERK1/2, and p38-MAPK in HRMECs.Conclusions: SC could inhibit laser-induced CNV formation via down-regulating VEGF expression and restrain the VEGF-induced tube formation and endothelial migration. Therefore, SC could be a potential candidate for the treatment of wet AMD.

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Section: Discussionsupporting

confidence: 93%

Section: Sanguinarine Chloride Suppressedmentioning

confidence: 99%

The Antiangiogenic Effect of Sanguinarine Chloride on Experimental Choroidal Neovacularization in Mice via Inhibiting Vascular Endothelial Growth Factor

Zhang

Mao

et al. 2021

Front. Pharmacol.

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“…40,41 Moreover, cataracts are directly related to the apoptosis of LECs caused by oxygen free radicals. 42,43 It has been reported that antioxidant genes and drugs can inhibit the oxidative damage caused by H 2 O 2 by reducing the activity of ROS. 44,45 Lens epithelial cells initiate apoptosis-related signal transduction pathways under oxidative stress, which mediates the apoptosis of LECs and promote the development of cataracts.…”

Section: Discussionmentioning

confidence: 99%

Echinatin mitigates H2O2-induced oxidative damage and apoptosis in lens epithelial cells via the Nrf2/HO-1 pathway

Ran¹,

Liu²,

Wu³

2021

Adv Clin Exp Med

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Background.Oxidative stress has been reported to be an early factor in the development of cataracts. Echinatin (Ech) is an active ingredient of licorice that exhibits antioxidant effects. Objectives.To investigate the effects of Ech on oxidative stress-induced lens epithelial cell (LEC) damage. Materials and methods.Human lens epithelial B3 cells (HLECs) were exposed to hydrogen peroxide (H 2 O 2 ) and were pretreated with or without Ech. For rescue experiments, ML385, an inhibitor of the Nrf2 pathway, was added into the medium.Results. Echinatin reversed the H 2 O 2 -induced reduction of cell viability in B3 cells. Additionally, H 2 O 2 induced oxidative stress, evidenced by an increase of reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and a decrease in superoxide dismutase (SOD) and catalase (CAT) levels, which could be abolished by Ech. Echinatin treatment also reduced HLEC apoptosis induced by H 2 O 2 . In addition, Ech pretreatment promoted Bcl-2 expression, and suppressed Bax and caspase-3 expression levels, in H 2 O 2 -treated B3 cells. Moreover, H 2 O 2 significantly reduced Nrf2 nuclear localization, as well as HO-1 and NQO1 expression, which could be reversed by Ech. Inhibition of Nrf2 by ML385 aggravated H 2 O 2 -induced oxidative damage and apoptosis in HLECs, and the protective effects of Ech on H 2 O 2 -induced oxidative damage and apoptosis could be restored by ML385. Conclusions.Echinatin mitigates H 2 O 2 -induced oxidative damage and apoptosis in HLECs via the Nrf2/HO-1 pathway, suggesting that Ech may be a potential drug for the treatment of cataracts.

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“…The p38 mitogen activated protein kinase (MAPK) signaling pathway, activated by oxidase stress, cytokines, and growth factors, plays a crucial role in controlling growth, apoptosis, and differentiation (Cuadrado and Nebreda, 2010). Multiple factors have been shown to affect oxidative stress and cell apoptosis via the p38 MAPK signaling pathway in HLECs and cataract tissues (Zhou and Menko, 2004;Huang et al, 2014;Bai et al, 2015;Ji et al, 2016;Gong et al, 2018;Zhang and Huang, 2019). We have previously reported that CRTAC1 knockdown significantly attenuated UVB-induced apoptosis and decreased p38 phosphorylation in HLECs ( Ji et al, 2016).…”

Section: Figmentioning

confidence: 99%

NF-κB/Cartilage Acidic Protein 1 Promotes Ultraviolet B Irradiation-Induced Apoptosis of Human Lens Epithelial Cells

Sun

Xiao

et al. 2020

DNA and Cell Biology

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The apoptosis of human lens epithelial cells (HLECs) is a characteristic change that occurs during the development of cataracts. Ultraviolet B (UVB) is known to induce the generation of reactive oxygen species (ROS) and apoptosis in HLECs, and thus cause cataracts. Previously, we reported the functions of cartilage acidic protein 1 (CRTAC1) in UVB-treated HLECs. However, the underlying mechanism was not known. In this study, we found that CRTAC1 expression and nuclear factor-kappa B (NF-kB) p65 nuclear translocation were elevated in capsule tissues of cataract patients in comparison with normal controls. The NF-kB inhibitor, pyrrolidine dithiocarbamate (PDTC), alleviated UVB-induced apoptosis in HLECs; while activation of NF-kB suppressed the effects of the ROS inhibitor, N-acetyl-L-cysteine (NAC), on UVB-treated HLECs. The expression and promoter activity of CRTAC1 was inhibited by PDTC and NAC. Moreover, the suppressed effects of CRTAC1 knockdown on UVB-induced ROS generation, cell apoptosis, nuclear translocation of NF-kB p65, and p38 phosphorylation were attenuated by a p38 agonist. In contrast, the p38 inhibitor abolished the promotional effects of CRTAC1 overexpression on HLECs. Taken together, our results for the first time show that NF-kB is a potential transcription factor for CRTAC1. The regulatory network involving NF-kB, CRTAC1, and p38 may therefore play an important role in cataract formation.

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Sanguinarine induces apoptosis of human lens epithelial cells by increasing reactive oxygen species via the MAPK signaling pathway

Cited by 12 publications

References 42 publications

The Antiangiogenic Effect of Sanguinarine Chloride on Experimental Choroidal Neovacularization in Mice via Inhibiting Vascular Endothelial Growth Factor

The Antiangiogenic Effect of Sanguinarine Chloride on Experimental Choroidal Neovacularization in Mice via Inhibiting Vascular Endothelial Growth Factor

Echinatin mitigates H2O2-induced oxidative damage and apoptosis in lens epithelial cells via the Nrf2/HO-1 pathway

NF-κB/Cartilage Acidic Protein 1 Promotes Ultraviolet B Irradiation-Induced Apoptosis of Human Lens Epithelial Cells

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