Nitric oxide donors as neuroprotective agents after an ischemic stroke-related inflammatory reaction.

摘要: Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption cellular homeostasis structural damage ischemic brain tissue. also triggers acute inflammation, exacerbates primary damage. Therefore, reducing oxidative stress (OS) downregulating inflammatory response are options that merit consideration as potential therapeutic targets for stroke. Consequently, agents capable modulating both elements will constitute promising solutions because clinically effective neuroprotectants have not yet been discovered no specific therapy stroke is available date. Because their ability modulate response, much attention has focused on role nitric oxide donors (NOD) neuroprotective in pathophysiology cerebral ischemia-reperfusion injury. Given short window, NOD appears be appropriate use during neurosurgical procedures involving transient arterial occlusions, or very early treatment stroke, possibly complementary neurodegenerative diseases such Parkinson Alzheimer, where an important promoter In present paper, we focus possible ischemia/reperfusion treatment.