MicroRNA-124 Prevents H&lt;sub&gt;2&lt;/sub&gt;O&lt;sub&gt;2&lt;/sub&gt;-Induced Apoptosis and Oxidative Stress in Human Lens Epithelial Cells via Inhibition of the NF-κB Signaling Pathway

Gu, Xiuli

doi:10.1159/000491433

Cited by 18 publications

(8 citation statements)

References 38 publications

(41 reference statements)

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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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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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“…Decreases in GSH-Px activity and exhaustion of GSH could increase injuries to the antioxidant system, ultimately resulting in lens epithelial cell apoptosis. Previous studies proposed that Bax, Bcl-2, and caspase-3 were related to the apoptotic process (Gu, 2018). Bax is a member of the Bcl-2 family that promotes apoptosis and increases in the Bax and Bcl-2 ratio promote cell apoptosis (Du et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Lanosterol Synthase Up-Regulation in UV-B-Induced Oxidative Stress

et al. 2019

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UV-B radiation may be an important risk factor in cataract etiology. After exposure to UV-B radiation, cells show imbalances in the repair of DNA damage, which induce changes in the levels of certain proteins, including alpha-crystallin, which is the most abundant protein in the lens and crucial for the maintenance of lens transparency. Lanosterol synthase (LSS), an essential rate-limiting enzyme in cholesterol biosynthesis, might play significant roles in oxidative stress and in the maintenance of lens transparency. However, the roles of LSS in UV-B-induced apoptosis are not well understood. Therefore, we irradiated female Sprague-Dawley rats with ultraviolet radiation to establish an animal model for exploring the variations in LSS expression during the early stages of UV-B exposure. In addition, we cultured human lens epithelial (HLE) cells that overexpress LSS and exposed them to UV-B radiation to explore the function of increased LSS expression in UV-B-induced apoptosis. The data demonstrated that UV-B exposure induced oxidative stress and apoptosis in rat lens epithelial cells and that irradiance exposure increased the level of lenticular damage. Additionally, UV-B exposure decreased the alpha-crystallin content and increased the expressions of Bax and cleaved caspase-3 compared with the control levels. After exposure to UV-B, the apoptosis-related index of HLE cells overexpressing LSS was lower than that of the control cells. Furthermore, ROS overproduction might activate the sirtuin 1 (Sirt1) pathway, which induced protein expressions of sterol regulatory element-binding transcription factor 2 (SREBF2), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), and LSS. However, the specific mechanism of the Sirt1 pathway needed to be further studied. In summary, UV-B exposure induced oxidative injury and resulted in crystallin denaturation and apoptosis in lens epithelial cells, and LSS might play a protective role during the early stages of this process and could be an important target in the cataract prevention.

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“…Downregulation of miRNA-155 ameliorates high-glucose-induced endothelial injury by inhibiting NF-κB activation and promoting HO-1 and NO production [71]. Gu revealed that miRNA-124 prevents H 2 O 2 -induced oxidative stress and apoptosis in human lens epithelial cells by suppressing the activation of the NF-κB pathway [85]. Results of Wei et al indicated that NF-κB positively regulated miRNA-21 expression under oxidative stress, and programmed cell death protein 4 (PDCD4) was a direct target for miRNA-21 [86].…”

Section: Nf-κb Pathwaymentioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

125

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Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases.

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MicroRNA-124 Prevents H<sub>2</sub>O<sub>2</sub>-Induced Apoptosis and Oxidative Stress in Human Lens Epithelial Cells via Inhibition of the NF-κB Signaling Pathway

Cited by 18 publications

References 38 publications

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

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

Protective Effects of Lanosterol Synthase Up-Regulation in UV-B-Induced Oxidative Stress

Oxidative Stress-Responsive MicroRNAs in Heart Injury

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