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- W2799710080 abstract "Objectives In the brain, glutamate is the most important excitable neurotransmitter in physiological and pathological conditions. However, the high level of glutamate induces neuronal cell death due to exitotoxicity and oxidative stress. The present study investigated to evaluate a possible neuroprotective effect of furosin isolated from Euphorbia helioscopia against glutamate-induced HT22 cell death. Methods Furosin was isolated from methanol extract of Euphorbia helioscopia and examined whether it protects glutamate-induced neuronal cell death. The cell viability was determined using Ez-Cytox assay. Anti-oxidative effect of furosin was determined by DPPH scavenging activities, and the levels of intracellular reactive oxygen species (ROS) were determined by the fluorescent intensity after staining the cells with H2DCFDA. To evaluate apoptotic cell death, we performed nuclear staining and image-based cytometeric analysis. Results The cell viability was significantly increased by treatement with furosin compared with the treatment with glutamate. Furosin showed a strong DPPH radical scavenging activity (EC50=1.83 μM) and prevented the accumulation of intra cellular ROS. Finally, the presence of 50 and 100 μM furosin significantly the percentage of apoptotic cells compared with glutamate treatment. Conclusion The present study found that furosin is a potent neuroprotectant against glutamate-induced oxidative stress through inhibition of apoptotic cell death induced by glutamate. Therefore, the present study suggests that furosin as a bioactive compound of E. helioscopia can be a useful source to develop a drug for the treatment of neurodegenerative diseases and acute brain injuries. Keywords: Furosin, Euphorbia helioscopia, Glutamate, Apoptotic cell death, HT22 cells" @default.
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- W2799710080 date "2018-03-31" @default.
- W2799710080 modified "2023-10-16" @default.
- W2799710080 title "Protective effect of furosin isolated from Euphorbia helioscopia against glutamate-induced HT22 cell death" @default.
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- W2799710080 doi "https://doi.org/10.13048/jkm.18004" @default.
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