Abstract
There is increasing evidence pointing toward the role of inflammatory processes in epileptic seizures, and reciprocally, prolonged seizures induce more inflammation in the brain. In this regard, effective strategies to control epilepsy resulting from neuroinflammation could be targeted. Based on the available data, preconditioning (PC) with low dose lipopolysaccharide (LPS) through the regulation of the TLR4 signaling pathway provides neuroprotection against subsequent challenge with injury in the brain. To test this, we examined the effects of a single and chronic brain LPS PC, which is expected to lead to reduction of inflammation against epileptic seizures induced by electroconvulsive shock (ECS). A total of 60 male Sprague Dawley rats were randomly assigned to five groups: control, vehicle (single and chronic), and LPS PC (single and chronic). We first recorded the data regarding the behavioral and histological changes. We further investigated the alterations of gene and protein expression of important mediators in relation to TLR4 and inflammatory signaling pathways. Interestingly, significant increased presence of NFκB inhibitors [Src homology 2-containing inositol phosphatase-1 (SHIP1) and Toll interacting protein (TOLLIP)] was observed in LPS-preconditioned animals. This result was also associated with over-expression of IRF3 activity and anti-inflammatory markers, along with down-regulation of pro-inflammatory mediators. Summarizing, the analysis revealed that PC with LPS prior to seizure induction may have a neuroprotective effect possibly by reprogramming the signaling response to injury.
Highlights
A series of complex events are believed to trigger subsequent changes in the brain causing epilepsy
Our observations indicated significant reduction in the duration of seizures induced by electroconvulsive shock (ECS) in single and chronic preconditioned groups compared to the vehicle animals (Figure 2)
As all animals in the ECS model were evoked immediately after receiving shock, the seizure latency was not observed in this model. (The latency was defined as the time of onset of the first tonic–clonic seizures in ECS-induced animals.) during our behavioral observation, administration of ECS exhibited high scores of tonic–clonic seizures, there was no mortality in the ECS-treated groups
Summary
A series of complex events are believed to trigger subsequent changes in the brain causing epilepsy. Inflammatory processes in cell injury resulting from prolonged seizures trigger molecular and cellular alterations, which leads to the production of vast numbers of different pro-inflammatory mediators (Amhaoul et al, 2015; Vezzani et al, 2016). In this regard, it is believed that neuroinflammation can be both a consequence and a cause of epileptic seizures (Amhaoul et al, 2015; Gershen et al, 2015). It is necessary to seek and explore novel and potential treatments for prevention of seizures in patients with epilepsy
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