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.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Han Z,Gao LY,Lin YH,Chang L,Wu HY,Luo CX,Zhu DYdoi
10.1016/j.ejphar.2016.03.006subject
Has Abstractpub_date
2016-04-15 00:00:00pages
129-35eissn
0014-2999issn
1879-0712pii
S0014-2999(16)30117-0journal_volume
777pub_type
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