ArticleMolecular neurobiology2025
Enoxaparin Protects C6 Glioma Cells from Glutamate-Induced Cytotoxicity by Reducing Oxidative Stress and Apoptosis.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Investigating the Effect of Low Molecular Weight Heparin, Enoxaparin, on Pentylenetetrazole (PTZ)-Induced Neuronal Damage in C6 and HT-22 Cell Lines.Cell biochemistry and biophysics · 2026Article
- Combating posterior capsular opacification: From conventional intraocular lens modifications to proactive defense via interface engineering.Materials today. Bio · 2026Review
- A novel modulator of the Axin/β-Catenin interaction to restore EAAT2 expression in alzheimer's disease: an in-silico and in-vitro approach.Metabolic brain disease · 2025Article
- Astaxanthin promotes apoptosis by suppressing growth signaling pathways in HT-29 colorectal cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Esomeprazole Potentiates the Cytotoxic Effects of Cisplatin in Gastric Carcinoma Cells.Journal of biochemical and molecular toxicology · 2025Article
- Investigation of the antitumor activity of lapatinib and NNC 55-0396 dihydrochloride combination in gastric adenocarcinoma.Medical oncology (Northwood, London, England) · 2025Article
- Investigating the antiproliferative mechanisms of NaHS, a hydrogen sulfide donor, in the SH-SY5Y cell line.Medical oncology (Northwood, London, England) · 2025Article
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Authors and funding
5 authors.
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Abstract
Recent studies suggest enoxaparin may protect the central nervous system (CNS) from damage. However, its specific effects on glial cells and the underlying mechanisms involving cell death and oxidative stress require further investigation. Therefore, this research investigated enoxaparin's potential to safeguard C6 glioma cells against glutamate-induced cytotoxicity, specifically focusing on its influence on oxidative stress and apoptotic mechanisms. To investigate the neuroprotective effects of enoxaparin against glutamate-induced cytotoxicity in C6 cells, four groups were established: a control group, a group exposed to 10 mM glutamate, a group treated with enoxaparin at concentrations ranging from 25 to 200 µM, and a group receiving both 10 mM glutamate and enoxaparin at concentrations ranging from 25 to 200 µM. Cell viability was measured using an XTT assay. To evaluate the effects of enoxaparin on oxidative stress, superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured using ELISA, along with total antioxidant status (TAS) and total oxidant status (TOS). Apoptosis was evaluated using flow cytometry, and caspase-3 activity, a key marker of apoptosis, was assessed using caspase-3 immunofluorescence staining. Enoxaparin at 50, 100, and 200 µM markedly increased cell viability in the enoxaparin + glutamate group. Enoxaparin treatment in the enoxaparin + glutamate group also significantly elevated levels of SOD and TAS, while concurrently decreasing MDA and TOS levels. These changes indicate a reduction in oxidative stress. Enoxaparin treatment further resulted in a significant decline in cleaved caspase-3 levels, a marker of apoptosis. Enoxaparin pre-treatment reduced cell death according to flow cytometry analysis. This study suggests enoxaparin's potential to shield C6 glioma cells from glutamate-induced cell death by mitigating both oxidative stress and apoptotic pathways. More research is needed to confirm this effect.
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