Abstract

There is a need to investigate the role of nuclear factor kappa B in the regulation of cyclooxygenase-2 expression in the epileptic rat brain and cultured hippocampal neurons. Immunofluorescence and polymerase chain reaction was used to detect the expression of nuclear factor kappa B and cyclooxygenase-2. In cultured hippocampal neurons and rat brain: the control group compared with the normal group, nuclear factor kappa B expression in the hippocampal dentate gyrus, cerebral cortex, the piriform cortex brain regions were significantly increased (P < 0.01). This is accompanied by a significant increase in cyclooxygenase-2 protein and mRNA expressions in the hippocampus (P < 0.01). In the experimental group compared to the control group, the nuclear factor-kappa B expression in the hippocampal dentate gyrus, cerebral cortex, piriform cortex, and other brain regions was significantly lower (P < 0.01), with the accompanying decrease in cyclooxygenase-2 protein and mRNA expression (P < 0.01) in the hippocampus. In conclusion, κB-decoy can inhibit nuclear factor kappa B activation in epileptic rat brain and cyclooxygenase-2 overexpression.

Highlights

  • Epilepsy is a serious disease of the nervous system

  • The results show that the expression of COX-2 can be changed either by activating or inhibiting the activity of NF-κB in cultured hippocampal neurons as well as epileptic rat brain

  • While the expression of NF-κB was significantly decreased in the experimental group compared with the control group, these results indicate that κB-decoy is effective in inhibiting the activation of NFκB in neurons of epilepsy-related brain areas

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Summary

Introduction

Epilepsy is a serious disease of the nervous system. Repeated seizures cause brain damage in people with epilepsy. It has been revealed that the inflammatory reaction induced by seizures is one of the reasons for the pathological changes in the brain, especially hippocampal sclerosis, including neuronal loss, glial cells proliferation, abnormal mossy fiber sprouting, and so on (Samland et al, 2003). The brain tissue of epileptic patients undergoing surgical resection shows strong inflammatory response, including up-regulation of IL-1β, TNF-α, and IL-6 and other pro-inflammatory factors (Deng et al, 2019). Recent reports showed that the inflammatory reaction is closely correlated with cyclooxygenase-2 (COX-2) overexpression and increased levels of prostaglandin. COX-2 is the rate-limiting enzyme of PGs (prostaglandins) that has a close relationship with inflammatory disease, which causes oxidative stress reaction and can convert arachidonic acid to PGs when activated. COX-2 can be regulated by promoting inflammatory factors as well as some growth factors related to an inflammatory reaction, the mechanism is still unclear

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