ArticleFrontiers in neurology2022
The Role of the Negative Regulation of Microglia-Mediated Neuroinflammation in Improving Emotional Behavior After Epileptic Seizures.
Article in Frontiers in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Kisspeptin System: A Modulator of Neuroinflammation and Behaviour in Temporal Lobe Epileptic Rats.Molecular neurobiology · 2026Article
- Apoptosis and Glial Marker Profiles in Hippocampus and Amygdala of Medically Intractable Temporal Lobe Epilepsy.Journal of cellular and molecular medicine · 2026Article
- Analysis of Serum VCAN-AS1 Expression Level in Patients with Cerebral Infarction Secondary Epilepsy and Its Mechanism by Regulating miR-885-3p/NTNG1.Neurochemical research · 2026Article
- Microglial phagocytosis in epilepsy: Mechanisms and impact.The Journal of physiology · 2026Review
- Polysaccharide-rich birch sap attenuates kainic acid-induced acute seizures by suppressing TLR4/NF-κB-mediated inflammation and preserving blood-brain barrier and glutamate homeostasis.Frontiers in pharmacology · 2026Article
- Review
- Research progress on the role of inflammatory mediators in the pathogenesis of epilepsy.Ibrain · 2025Review
- Identification of TIMP1 as an inflammatory biomarker associated with temporal lobe epilepsy based on integrated bioinformatics and experimental analyses.Journal of neuroinflammation · 2023Article
- Neuroprotective Effects of Early TLR4 Blockade with Compound C34 in Temporal Lobe Epilepsy: Alleviation of Neuroinflammation and Apoptosis.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Objective: Studies have long shown that uncontrolled inflammatory responses in the brain play a key role in epilepsy pathogenesis. Microglias play an important role in epileptic-induced neuroinflammation, but their role after epileptic seizures is still poorly understood. Alleviating epilepsy and its comorbidities has become a key area of interest for pediatricians. Methods: A pilocarpine-induced rat model of epilepsy was established. The rats were randomly divided into four groups: a control group, epilepsy group, TLR4 inhibitor group (epilepsy+TAK-242), and NF-κB antagonist group (epilepsy+BAY11-7082). Results: 1. The results of TUNEL staining showed that the expression in rats in the epilepsy group was the most obvious and was significantly different from that in rats in the control, EP+BAY and EP+TAK groups. 2. The expression of TLR4 and NF-κB was highest in rats in the epilepsy group and was significantly different from that in rats in the control, EP+BAY and EP+TAK groups. 3. The fluorescence intensity and number of IBA-1-positive cells in rats in the epilepsy group were highest and significantly different from those in rats in the control, EP+BAY and EP+TAK groups. Western blot analysis of IBA-1 showed that the expression in rats in the epilepsy group was the highest and was statistically significant. 4. CD68 was the highest in rats in the epilepsy group and was statistically significant. 5. In the open-field experiment, the central region residence time of rats in the EP group was delayed, the central region movement distance traveled was prolonged, the total distance traveled was prolonged, and the average speed was increased. Compared with rats in the EP group, rats in the EP+BAY and EP+ TAK groups exhibited improvements to different degrees. Conclusion: At the tissue level, downregulation of the TLR4/NF-κB inflammatory pathway in epilepsy could inhibit microglial activation and the expression of the inflammatory factor CD68, could inhibit hyperphagocytosis, and inhibit the occurrence and exacerbation of epilepsy, thus improving cognitive and emotional disorders after epileptic seizures.
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