ArticleNeurochemical research2026
STING Mediates Microglial Polarization to Promote Neuroinflammation in Epilepsy-Related Cognitive Dysfunction.
Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Epilepsy is a chronic neurological disorder characterized by recurrent seizures and frequently accompanied by cognitive deficits for which effective treatments are lacking. Neuroinflammation, particularly microglia-mediated immune responses, is pivotal in epileptogenesis. Although the stimulator of interferon genes (STING) pathway is a key cytosolic DNA-sensing mechanism driving innate immunity, its specific role in epilepsy-related cognitive dysfunction remains unclear. This study investigated the function of the STING pathway in epilepsy pathology and its therapeutic potential. Adult male Sprague-Dawley rats (250-300 g) were subjected to lithium chloride-pilocarpine-induced status epilepticus (SE). The study consisted of two parts. In the first part, the temporal expression of hippocampal STING was examined at 1, 3, 7, 14, and 30 days after SE. In the second part, rats were randomly divided into control (Con+Vehicle), epilepsy (EP+Vehicle), and C-176-treated (EP + C-176) groups. Vehicle (1000 µL) or C-176 (2 mg/rat in 1000 µL) was administered intraperitoneally once daily from 1 day before SE to 6 days after SE. Seizure severity was assessed using the Racine scale. Hippocampal tissues were collected on day 7 after SE for analysis, and cognitive function was evaluated by the Morris water maze test on days 30-35 after SE. The results showed that hippocampal STING expression peaked on day 7 after SE compared with the control group, accompanied by cytosolic double-stranded DNA (dsDNA) accumulation and a shift of microglia toward a pro-inflammatory M1 phenotype. C-176 treatment significantly inhibited STING expression, reduced p-TBK1 and p-NF-κB p65 levels, reversed M1 microglial polarization with decreased iNOS and increased Arg-1 expression, decreased levels of pro-inflammatory cytokines (including IL-6, cleaved IL-1β, and TNF-α), attenuated neuronal damage, and improved learning and memory in SE rats. Our findings suggest that status epilepticus induces neuronal injury and dsDNA release, activating the STING pathway in microglia and driving neuroinflammation via the TBK1/NF-κB axis, leading to cognitive dysfunction. Inhibiting STING alleviates these effects by promoting microglial phenotypic switching from M1 to M2 via regulation of the TBK1/NF-κB pathway. This study identifies STING as a critical regulator of neuroinflammation and a novel therapeutic target for epilepsy-related cognitive dysfunction.
Indexed as
Identifiers
41880095What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.