Alleviation of Oxidative Damage and Involvement of Nrf2-ARE Pathway in Mesodopaminergic System and Hippocampus of Status Epilepticus Rats Pretreated by Intranasal Pentoxifylline.
XRN2 and PAPD4 levels did not change in calretinin- and CamKII-positive cells, although it was possible to determine that PAPD4, but not XRN2, was upregulated in parvalbumin-positive cells, revealing that SE induction unbalances the accumulation of these functional-opposed proteins in inhibitory interneurons that directly innervate distinct domains of pyramidal cells.
Early WP1066 administration reduces known downstream targets of STAT3 transcription 24h after SE including cyclin D1 and mcl-1 levels, known for their roles in cell-cycle progression and cell survival, respectively.
The temporal time change and distribution of p-DARPP-32 suggest that phosphorylation of DARPP-32 may be involved in PTZ-induced epilepsy in rat brain including cortex, hippocampus and striatum, and p-DARPP-32 may play a central role in the onset of SE.
We measured blood plasma levels of the inflammation markers interleukin 1β (IL-1β), interleukin 6 (IL-6), by enzyme-linked immunosorbent assays (ELISAs) and C-reactive protein (CRP) by immunoturbidimetry, at 1 day after SE (acute period), at 1 week (during the latent period), and at 2 months after SE, which is the chronic epileptic phase when spontaneous seizures occur.
Peroxisome proliferator-activated receptors γ/mitochondrial uncoupling protein 2 signaling protects against seizure-induced neuronal cell death in the hippocampus following experimental status epilepticus.
Our data indicated that MIP-1α as a regulator, linking with the CCR5 receptor, may be involved within the early stages of the epileptogenic process following SE by i.c.v.KA injection.
Increased expression of the chemokines CXCL1 and MIP-1α by resident brain cells precedes neutrophil infiltration in the brain following prolonged soman-induced status epilepticus in rats.
Expression of CCL3 and CCL4 proteins was elevated in astrocytes in the enthorinal and piriform cortices, amygdala, and hippocampus showing the largest increase at 4D after status epilepticus.
Real-time quantitative PCR analysis of gene expression revealed that a significant 33% reduction of transcripts for Kv3.4 (gene Kcnc4) occurred after 1 month of pilocarpine-induced status epilepticus and persisted during the chronic phase of the model.
Gene expression of Hsd11b1 (cortisol generating enzyme) was significantly higher in epileptic versus control rats at 24h and 2 months, after induction of SE.
With as little as a 5 min duration of status epilepticus (SE), γ-H2AX increased in CA1, CA3, and entorhinal cortex to a greater extent than that observed after the clusters of individual seizures, with still greater increases after 120 min of SE.