In contrast, treatment with the PPAR�� antagonist, GW9662 exerted

In contrast, treatment with the PPAR�� antagonist, GW9662 exerted opposite effects. Thus, the present study provided a novel demonstration of an antioxidant role for the PPAR�� UCP2 signaling pathway against oxidative stress and mitochondrial dys functions that reduced neuronal cell injury in the hippo campal CA3 subfield after the experimental model of temporal lobe status epilepticus. Neuroprotection meanwhile following prolonged seizures, such as status epilepticus should encompass not only the pre vention of neuronal cell death, but also preservation of neuronal and network function. Less well studied are the protective mechanisms elicited by seizure activity espe cially under status epilepticus. Except for the detrimental chain reaction under status epilepticus, acute response protein to counteract these detrimental effects may be elicited as an endogenous protective mechanism.

En dogenous neuronal survival mechanisms following pro longed seizure insult are those that have been evolutionarily conserved and may trigger a number of signaling pathways to Inhibitors,Modulators,Libraries exert the protective effect and therefore be strong candidates to imply as therapeutic Inhibitors,Modulators,Libraries strategies. In animal studies with status epilepticus, several endogenous protective mechanisms to lessen neuronal damage were proposed, including activation ERK1 2, epileptic tolerance, vascular endothelial growth factor, activation of adenosine A1 receptors, erythropoi etin receptor. Based on real time PCR and west ern blot analyses, we demonstrated a significant increase in UCP2 mRNA in the hippocampal CA3 subfield after KA elicited status epilepticus, followed by augmented UCP2 protein levels.

In addition, immunofluorescence staining demonstrated that the activated UCP2 was mainly in the mitochondria of hippocampal CA3 neu rons. Thus, our results suggested that mitochondrial UCP2 may play an endogenous neuroprotective role against hippocampal neuronal cell damage under the stress of prolonged Inhibitors,Modulators,Libraries epileptic seizures. Several antioxidant systems are present in the cell to counteract oxidative stress and to restore redox balance, and may be considered endogenous protective mechanisms under pathological conditions. In addition to the documen ted ROS detoxifying enzymes and low molecular weight antioxidants, whether mitochondrial UCP functions as a natural antioxidant defense mechanism against oxidative stress is still debatable.

Mitochondrial UCPs control the leakage of protons across the inner mitochondrial mem brane and have emerged as Inhibitors,Modulators,Libraries an important Inhibitors,Modulators,Libraries modulator for oxidative stress. As UCP2 are most prevalent selleck Ganetespib in the nervous system, and a majority of the neurodegenerative disorders engages free radical production, it is reasonable to propose that UCP2 induction will be involved in these neurological disorders, including status epilepticus.

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>