Conclusions In conclusion, our results reveal that sPLA2 IIA activates primary and immortalized BV 2 microglia cells, EGFR plays a key role as a critical regulator of this sPLA2 http://www.selleckchem.com/products/AP24534.html IIA mediated effect, and also indicates that shedding of pro Inhibitors,Modulators,Libraries HB EGF is a crucial step in this response. Accordingly, the possibility that sPLA2 IIA may affect immune system function in the CNS in certain pathologies should be carefully Inhibitors,Modulators,Libraries considered. Introduction Ischemic stroke is a highly disabling neurodegenerative condition with a high incidence in industrialized coun tries. Ischemic strokes in humans account for approximately 80% of all strokes and they are caused by thrombotic or embolic occlusion that decreases or suppresses the flow of blood in the middle cerebral artery, one of the main arteries supplying blood to the brain.

Brain injury following cerebral ischemia involves a complex succession of Inhibitors,Modulators,Libraries events that evolve spatially and temporally, causing varying degrees of cell damage depending on the characteristics of the initial insult. The ischemic core and the peri infarct zone suffer differing degrees of cellular damage, and it Inhibitors,Modulators,Libraries is widely accepted that cell death in the ischemic core is triggered by necrosis while that which occurs in the penumbra is predominantly mediated by apoptosis. As apoptosis is a reversible process, thera peutic interventions targeting this process have the poten tial to prevent or limit cell death in the peri infarct zone, even when applied post ischemia. MCA occlusion is a rodent model of ische mia that is widely used to analyze the mechanisms triggered by ischemic stroke and to study potential treat ments.

In this model, the cerebral cortex and the stri atum are most affected brain regions, while secondary cell death occurs in the Inhibitors,Modulators,Libraries hippocampus. Two types of MCAO stroke models are commonly used, transient ischemia with reperfusion and permanent ischemia without reperfusion. The latter is more similar to naturally occurring cerebral ischemia in humans and, thus, it is of greater selleck chemicals llc clinical relevance. Moreover, this model provides a useful means to test therapeutic approaches aimed at repairing the injured tissue in the late stages of cerebral ischemia. Estradiol is the main female sex hormone that, in addition to its classic role in reproduction, exerts po tent neurotrophic and neuroprotective effects in the brain. Strokes naturally occur less in females than in age matched males up to the age of 75 years, after which the incidence in women increases. A large body of evidences suggests that estradiol protects against brain injury and several neurodegenerative diseases. Indeed, physiological or pharma cological levels of estradiol administered prior to tMCAO or pMCAO reduce the area of ischemic damage in rodent models of stroke.