Spatial, temporal, and cell-type-specific expression of NADPH Oxidase isoforms following seizure models in rats

Specific inhibition of NADPH oxidase 2 modifies chronic epilepsy

“…To determine the effect of gp91ds-tat on NOX2 expression and NOX activity in-vivo , we analyzed brain samples at a time when NOX2 expression peaked in hippocampus of rats after status epilepticus (SE), i.e., 24 h post-SE [ 15 ]. Rats were first injected with kainic acid to induce SE.…”

“…Among the seven NOX isoforms, NOX2 was reported as the main isoform in brain tissues such as glia and neurons [ [31] , [32] , [33] ], and its activation has been linked to brain pathology, implying that NOX2-mediated ROS production participates in acute and chronic neurological disease [ 14 , 34 , 35 ]. Recently, we studied the spatial and temporal expression of NOX2 following the acute seizure model (induced by pentylenetetrazol) and following status epilepticus (SE) induced by systemic administration of kainic acid [ 15 ]. We demonstrated that NOX2 has a transient expression pattern in the cortex while in the hippocampus its expression was persistent for up to 1-week post-seizure [ 15 ].…”

“…The NOX2 mRNA level was determined by quantitative RT-PCR using our previously reported primers [ 15 ]. Total RNA from cortex and hippocampus were extracted using tri-Reagent (Sigma-Aldrich, St. Louis, MO, USA) and subsequently purity and quantity was determined by Nanodrop spectrophotometry (Nanodrop Technologies, Thermo, Waltham, MA, USA); and ratios of 260:280 were 1.8–2.0.…”

“…Several in vivo and in vitro studies demonstrated that NADPH Oxidase 2 (NOX2) is a primary source of ROS production, activated by N‐methyl‐ d ‐aspartate (NMDA) receptors, which leads to neuronal depolarization and increasing of the cytoplasmic Ca 2+ load, playing an essential role in epileptogenesis and eventually leading to neurodegeneration and cell death [ [10] , [11] , [12] , [13] , [14] ]. Recently, we have demonstrated that following pentylenetetrazol (PTZ) induced seizure, NOX2 expression in the cortex is decreased within 6 h then increased at 24 h post-seizure [ 15 ]. Interestingly, we found that in the hippocampus NOX2 was overexpressed for 1–7 days post-seizure.…”

“…Interestingly, we found that in the hippocampus NOX2 was overexpressed for 1–7 days post-seizure. Moreover, we found that NOX2 expression is increased up to 2 weeks following kainic acid induced status epilepticus (SE), in both cortex and hippocampus [ 15 ].…”