ArticleFrontiers in pharmacology2022
Emodin Protects SH-SY5Y Cells Against Zinc-Induced Synaptic Impairment and Oxidative Stress Through the ERK1/2 Pathway.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Emodin Suppresses the RAGE/ROCK1 Pathway to Modulate the Oligodendrocyte Lineage and Ameliorate Demyelination in Vascular Dementia Rats.CNS neuroscience & therapeutics · 2026Article
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Emodin, a Phytotherapeutic Anthraquinone, Potently Attenuates Synaptic Redox Pathology in Aged Rats.Degenerative neurological and neuromuscular disease · 2026Article
- A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma.Communications biology · 2025Article
- Investigating the Formation and Molecular Solubilization Mechanism of Emodin Solid Dispersions by Molecular Dynamics Simulation.Molecules (Basel, Switzerland) · 2025Article
- Emodin protects against severe acute pancreatitis-associated acute lung injury by activating Nrf2/HO-1/GPX4 signal and inhibiting ferroptosis in vivo and in vitro.BMC gastroenterology · 2025Article
- Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification.Frontiers in oncology · 2025Article
- The Activity of 1,8-Dihydroanthraquinone Derivatives in Nervous System Cancers.Molecules (Basel, Switzerland) · 2024Review
- NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Metabolic Derangement of Essential Transition Metals and Potential Antioxidant Therapies.International journal of molecular sciences · 2024Review
- A Review on Bioactive Anthraquinone and Derivatives as the Regulators for ROS.Molecules (Basel, Switzerland) · 2023Review
- Protective Effect ofMolecules (Basel, Switzerland) · 2023Article
- High-resolution atomic force microscopy as a tool for topographical mapping of surface budding.Frontiers in cell and developmental biology · 2022Article
- Rapamycin Attenuated Zinc-Induced Tau Phosphorylation and Oxidative Stress in Rats: Involvement of Dual mTOR/p70S6K and Nrf2/HO-1 Pathways.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc is an essential trace element important for the physiological function of the central nervous system. The abnormal accumulation of zinc inside neurons may induce mitochondrial dysfunction and oxidative stress, which contribute to many brain diseases. We hypothesized that natural anthraquinone derivative emodin can protect against neurotoxicity induced by pathological concentrations of zinc via the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and alleviate oxidative stress and mitochondrial dysfunction. Human neuroblastoma (SH-SY5Y 26 cells) was treated with zinc sulfate and different concentrations of emodin, and changes in the levels of ETK1/2 expression, oxidative stress (DCFH-DA staining), mitochondrial function (JC-1 staining), lipid peroxidation (4-hydroxynonenal staining), and DNA oxidation (8-hydroxy-2-deoxyguanosine staining) were examined. Emodin ameliorated zinc-induced altered expression of levels of phosphorylated ERK1/2 (not total ETK1/2) and synaptic proteins (presynaptic SNAP 25, synaptophysin and postsynaptic PSD95) in SH-SY5Y cells. Moreover, emodin inhibited the generation of reactive oxygen species and oxidative stress and facilitated the collapse of mitochondrial membrane potential (ΔΨm) in SH-SY5Y cells. In conclusion, our results indicated that emodin exerts neuroprotective effects against zinc by normalizing synaptic impairment by decreasing the phosphorylation of ERK1/2, reducing reactive oxygen species and protecting mitochondrial function.
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