ArticleCentral-European journal of immunology2022
Scopoletin protects retinal ganglion cells 5 from high glucose-induced injury in a cellular model of diabetic retinopathy via ROS-dependent p38 and JNK signaling cascade.
Article in Central-European journal of immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- GLP-1 receptor agonists in eye disease: a comprehensive review of current research and future potential.BMC ophthalmology · 2026 · on this mapPooled it
- Moscatilin alleviates oxidative stress and inflammatory response of Müller cells in diabetic retinopathy through suppressing the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase and nuclear factor kappa-B signaling pathways.Journal of cell communication and signaling · 2025Article
- Scopoletin: a review of its pharmacology, pharmacokinetics, and toxicity.Frontiers in pharmacology · 2024Review
- Angiogenic and Fibrogenic Dual-effect of Gremlin1 on Proliferative Diabetic Retinopathy.International journal of biological sciences · 2024Article
- Neuroprotective effects of idebenone on hydrogen peroxide-induced oxidative damage in retinal ganglion cells-5.International ophthalmology · 2023Article
- Neurovascular Cell Death and Therapeutic Strategies for Diabetic Retinopathy.International journal of molecular sciences · 2023Review
- Membrane Blue Dual Protects Retinal Pigment Epithelium Cells/Ganglion Cells-Like through Modulation of Mitochondria Function.Biomedicines · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protective activity of scopoletin (SPT) against glucose-induced cataract has been attributed to attenuation of aldose reductase activity and oxidative stress in a rat model. The present investigation was aimed to study the protective effect and mechanism of SPT in retinal ganglia cells (RGC) under oxidative stress and apoptosis induced by hyperglycemia. The RGC-5 cells were pre-conditioned with variable SPT concentrations for 6 hours and then subjected to hyperglycemia for 48 hours. The cell viability, mito- chondrial membrane potential (MMP) and oxidative stress markers were quantified. Western blotting was employed to screen the expression of mitogen-activated protein kinase (MAPK) and various apoptosis related proteins. SPT blocked the high-glucose induced cell injury and normalized the mitochondrial functioning via lowering the loss of MMP and release of cytochrome c. Pretreatment with SPT suppressed the enhanced ROS, malondialdehyde, and protein carbonyl content triggered by high-glucose exposure in RGC-5 cells. SPT normalized the apoptotic proteins in RGC-5 cells. The phosphorylation of c-Jun N-terminal kinases (JNK) and p38 MAPK in RGC-5 due to hyperglycemia was attenuated by SPT. Overall, SPT exhibited a protective effect in RGC-5 cells exposed to a high-glucose environment via its antioxidant efficacy, inhibition of apoptosis and modulation of the ROS-dependent p38/JNK signaling cascade.
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