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Neuroprotection of taurine against reactive oxygen species is associated with inhibiting NADPH oxidases
- Source :
- European Journal of Pharmacology. 777:129-135
- Publication Year :
- 2016
- Publisher :
- Elsevier BV, 2016.
-
Abstract
- It is well established that taurine shows potent protection against glutamate-induced injury to neurons in stroke. The neuroprotection may result from multiple mechanisms. Increasing evidences suggest that NADPH oxidases (Nox), the primary source of superoxide induced by N-methyl-d-aspartate (NMDA) receptor activation, are involved in the process of oxidative stress. We found that 100μM NMDA induced oxidative stress by increasing the reactive oxygen species level, which contributed to the cell death, in vitro. Neuron cultures pretreated with 25mM taurine showed lower percentage of death cells and declined reactive oxygen species level. Moreover, taurine attenuated Nox2/Nox4 protein expression and enzyme activity and declined intracellular calcium intensity during NMDA-induced neuron injury. Additionally, taurine also showed neuroprotection against H2O2-induced injury, accompanying with Nox inhibition. So, we suppose that protection of taurine against reactive oxygen species during NMDA-induced neuron injury is associated with Nox inhibition, probably in a calcium-dependent manner.
- Subjects :
- 0301 basic medicine
Taurine
N-Methylaspartate
Pharmacology
medicine.disease_cause
Neuroprotection
Calcium in biology
Mice
03 medical and health sciences
chemistry.chemical_compound
medicine
Animals
Enzyme Inhibitors
Neurons
chemistry.chemical_classification
Mice, Inbred ICR
Reactive oxygen species
NADPH oxidase
Cell Death
biology
Chemistry
Superoxide
NADPH Oxidases
NOX4
Hydrogen Peroxide
Up-Regulation
Oxidative Stress
Neuroprotective Agents
030104 developmental biology
nervous system
Biochemistry
biology.protein
Calcium
Reactive Oxygen Species
Oxidative stress
Subjects
Details
- ISSN :
- 00142999
- Volume :
- 777
- Database :
- OpenAIRE
- Journal :
- European Journal of Pharmacology
- Accession number :
- edsair.doi.dedup.....e2bdb4ce80e994d24a75cefe29acdf0f