＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

原钒酸钠；正钒酸钠

类白色固体

Soluble in DMSO, water, ethanol

(Na,K)-ATPase

In transient forebrain ischemia, Sodium orthovanadate rescues cells from delayed neuronal death in the hippocampal CA1 region. The neuroprotective effects of Sodium orthovanadate and IGF-1 are associated with preventing decreased Akt-Ser-473 phosphorylation in the CA1 region observed immediately after reperfusion. Akt is moderately activated in the cell bodies and dendrites of pyramidal neurons after orthovanadate treatment. The Sodium orthovanadate treatment also prevents the decrease in phosphorylation of mitogen-activated protein kinase (MAPK). Sodium orthovanadate inhibits ASK1 through the PI3-K/Akt-dependent pathway. Sodium orthovanadate up-regulates Akt activity in the brain and in turn rescue neurons from delayed neuronal death by inhibiting FKHR-dependent or -independent death signals in neurons.

In a rat model of myocardial ischemic infarction, sodium orthovanadate rescues cells from ischemia/reperfusion injuries. Post-treatment with Sodium orthovanadate reduces infarct size in a dose-dependent manner. Sodium orthovanadate treatment also ameliorates contractile dysfunction of the left ventricle 72 hours after reperfusion. The cytoprotective action of Sodium orthovanadate treatment is closely associated with inhibition of fodrin breakdown. Sodium orthovanadate treatment inhibits caspase-3 activation induced by ischemia.