ArticlePsychiatry and clinical psychopharmacology2025
Investigating the Effects of Vortioxetine in an Experimental Model of Autism Spectrum Disorder: Role of NOD-like Receptor Protein-3 Inflammasome Pathway.
Article in Psychiatry and clinical psychopharmacology, 2025. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: The aim of the present study was to investigate NOD-like receptor-3 (NLRP-3)-mediated inflammasome activation in macrophage and microglia cells, which is one of the early step mechanisms in the formation of proinflammatory cytokines, in an autism model and also investigate the possible effect of vortioxetine (VTX), which has a multimodal mechanism of action, in the treatment of autism in a valproic acid (VPA)-induced experimental rat model of autism spectrum disorder (ASD). Materials and Methods: Male Sprague-Dawley rats were divided into 3 groups: Control (n = 12), ASD (n = 16), and ASD + VTX (n = 16). The VTX (5 mg/kg/day) or saline was administered to the male offspring born from pregnant rats administered VPA (400 mg/kg) or saline, between postnatal 30-45 days. Open field, body splash, and social interaction tests were performed in groups on postnatal days 46-52. The NLRP3 inflammasome components such as NLRP3, caspase-1, and ASC levels were investigated in the prefrontal cortex by real-time polymerase chain reaction. Data were analyzed using 1- or 2-way analysis of variance (ANOVA) and Tukey's multiple comparison tests, and differences of P < .05 were considered statistically significant. Results: The ASD model showed increases in locomotor activity and repetitive behaviors like grooming despite decreases in sociability and social interactions. These findings as well as observational malformations supported the formation of an autism model. It was found that sniffing and following behaviors as social interaction markers were significantly increased and avoidance behavior was reduced with VTX treatment. In molecular analyses, NLRP3 inflammasome components, NLRP3, ASC, and caspase-1 were increased in the ASD model. It was observed that VTX treatment statistically significantly reduced the increased NLRP3, caspase-1, and ASC gene expressions in ASD. Conclusion: In light of the findings of the study, it was thought that the NLRP-3 pathway may have an important role in the neurobiology of ASD. VTX, as a multimodal antidepressant, has some beneficial effects for the improvement of the behavioral and molecular parameters of ASD.
Identifiers
What 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.