Table 1.

Enhancement of NO^• production and NOS inhibitor-based therapies. Pretreatment indicates that the compound was administered before experimental ischemia; posttreatment indicates that the compound was administered after the episode. MCAO—middle cerebral artery occlusion, ODG—oxygen and glucose deprivation.

	Compound	Effect
NO Donors
Pretreatment	LA-419	in vivo: −reduced iNOS, nNOS, nitrotyrosine expression and increased apparent diffusion coefficient in endothelin-1-induced focal cerebral ischemia or global cerebral ischemia model in rats induced by oxygen and glucose deprivation	[156,157]
	GSNO	in vivo: −reduced caspase-3, -8, -9, tBID cleavage in global ischemia models in rats −increased Bid, pro-caspase-3 and pro-caspase-9 expression in global ischemia model in rats −reduced Fas, CaMKII, MKK4 S-nitrosylation, increased nNOS S-nitrosylation and phosphorylation, increased CaMKII phosphorylation in global ischemia models in rats −increased cell density in CA1 in global ischemia models in rats −reduced infarct size and edema in MCAO model in mice	[169,170,171,172]
	ZJM-289	in vitro: −increased cell viability in primary cortical neuron in OGD model −reduced mitochondrial dysfunction in primary cortical neuron in OGD model −decreased Ca2+ release and ROS production in primary cortical neuron in OGD model in vivo: −reduced infarct size and edema and improved neurologic deficit in MCAO model in rats	[155,173]
	SIN-1	in vivo: −no influence or reduced infarct size in MCAO model in rats	[174,175]
	DETA NONOate	in vivo: −no influence on infarct size in MCAO model in rats	[174]
	NBP	in vitro: −increased cell viability in primary cortical neuron in OGD model −reduced mitochondrial dysfunction in primary cortical neuron in OGD model −decreased Ca2+ release and ROS production in primary cortical neuron in OGD model in vivo: −reduced infarct size and improved neurologic deficit in MCAO model in rats	[173,176]
	Spermine NONOate	in vivo: −reduced infarct size in MCAO model in rats −increased cortical perfusion in MCAO model in rats	[152]
	sodium nitroprusside	in vivo: −reduced infarct size in MCAO model in rats	[152]
Posttreatment	GSNO	in vivo: −reduced infarct size	[171]
	DETA NONOate	in vivo: −no influence on infarct size in MCAO model in rats −improved neurologic deficit and increased cGMP level in MCAO model in rats −increased cell proliferation in subventricular zone, olfactory bulb and dentate gyrus in MCAO model in rats	[150]
	SIN-1	in vivo: −reduced infarct size in MCAO model in rats	[153,154]
	sodium nitroprusside	in vivo: −reduced infarct size in MCAO model in rats	[153]
NOS or nNOS inhibitors
Pretreatment	7-NI	in vivo: −increased nNOS S-nitrosylation and phosphorylation, decreased CaMKII and MKK4 S-nitrosylation and increased CaMKII phosphorylation in global ischemia model or MCAO in rats −decreased caspase-3 cleavage in MCAO model in rats −increased cell density in CA1 in global ischemia model or MCAO model in rats −reduced maximal NO concentration in bilateral common carotid artery occlusion in rats	[170,172,177]
	L-NAME	in vivo: −reduced infarct size and improved neurological deficit in MCAO model in rats −reduced glutamate, aspartate, glutamine synthetase and nitrate/nitrite level in MCAO model in rats −increased ATP and NAD level in MCAO model in rats −reduced TNF-α expression and increased IL-10 expression in MCAO model in rats	[174,178]
Posttreatment	7-NI	in vivo: −reduced neuronal damage in global cerebra ischemia in rats	[179]
	L-NAME	in vivo: −reduced infarct volume in MCAO model in rats and mice −improved neurological deficit in MCAO model in rats and mice −reduced level of tissue nitric oxide end products in MCAO model in mice −reduced nitrate/nitrite level and increased NAD level in MCAO model in rats	[178,180]
iNOS inhibitors
Pretreatment	aminoguanidine	in vivo: −reduced infarct volume, edema, neurological deficits, necrotic cell death in penumbra and core and reduced apoptosis in penumbra in MCAO model in rats	[181]
Posttreatment	aminoguanidine	in vivo: −reduced infarct volume in permanent MCAO model in mice −reduced ischemia-induced neurogenesis in dentate gyrus in MCAO model in rats	[167,182,183]
	1400 W	in vivo: −reduced infarct size neurological deficit in MCAO model in rats −inhibited delayed increase in glutamate level in MCAO model in rats	[184]
	S-methylisothiorea	in vivo: −reduced neurological deficit, mortality, infarct volume ratio in MCAO model in rats −attenuated morphological changes in cortical neurons in MCAO model in rats	[185]