Our first series of experiments therefore, established that oxidative stress damages occurred in hippocampal CA3 neural cells following experimental lobe status epilepticus. We observed a significantly selleck chemicals llc heightened content of oxidized proteins in the ipsilateral hippo campal CA3 subfield as early as 3 h, followed by a progressive reduction over 24 h after unilateral microinjection of KA into the left CA3 area. We also observed a significant in crease in oxidized proteins in the contralateral CA3 subfield over the same time intervals after local ap plication of KA into the left hippocampal CA3 sub field. Importantly, the temporal changes of protein oxidations in the bilateral hippocampal CA3 subfield paralleled the time course of O2 production after ex perimental status epilepticus.

Inhibitors,Modulators,Libraries Temporal course of Bax and cytochrome c translocation Inhibitors,Modulators,Libraries in the hippocampal CA3 subfield following experimental temporal lobe status epilepticus Our second series of experiments investigated whether the Bcl 2, Bax and cytochrome c signaling cascades are associated with excessive ROS production in the hippo campal CA3 subfield following experimental temporal lobe status epilepticus. Western blot analysis revealed that Bcl 2 was not discernibly altered in either the mitochon drial or cytosolic fraction of samples obtained from the hippocampal CA3 subfield. However, there was a signifi cant decrease of Bax level and increase of cytochrome c level in the cytosolic fraction of samples from the bilateral hippocampal CA3 Inhibitors,Modulators,Libraries subfield after unilateral microinjection of KA into the left CA3 region, accompanied by a corresponding increase of Bax level and decrease of cytochrome c level in the mitochondrial fraction.

Of note is that this induced mitochondria bound translocation of Bax from the cytosol and cytosol bound translocation of cytochrome c from the mitochondria Inhibitors,Modulators,Libraries followed a time frame that started from 3 h in the ipsilateral and 6 h in the contralateral CA3 area, and was sustained 48 h after the induction of experimental temporal lobe status epilepticus. Temporal changes of PPAR�� and UCP2 expression in the hippocampal CA3 subfield following Inhibitors,Modulators,Libraries experimental temporal lobe status epilepticus Our third series of experiments examined whether PPAR�� and UCP2 in the hippocampal CA3 subfield exhibit changes in expression level following experimental tem poral lobe status epilepticus.

After unilateral microinjec tion of KA into the left CA3 region, western blot analysis revealed a slight decrease of PPAR�� 6 h after ipsilateral KA treatment, followed by a significant increase of expres sion from 12 to 48 h in the bilateral hippocampal CA3 subfields. More intriguingly, real time PCR analysis revealed that Ucp2 mRNA underwent a significant sellckchem increase in the bilateral hippocampal CA3 area that peaked at 6 h after the elicitation of sustained hippocampal seizure discharges.