ArticleIBRO neuroscience reports2025
N-acetyl cysteine through modulation of HDAC
Article in IBRO neuroscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- An Overview of Depression Pathogenesis: Prevailing Hypotheses and Associated Neurobiological Underpinnings Primarily Evidenced by Rodent Studies.Depression and anxiety · 2026Review
- N-acetyl Cysteine Reduces Behavioral Disorders of the First and Second-generation Weaned Mice through the Modulation of TAC and the DNMT1 Gene Expression in the Hippocampus.Current pharmaceutical design · 2026Article
- Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Social isolation stress (SIS) in early life can lead to behavioral disorders. N-acetylcysteine (NAC), an antioxidant, may aid treatment. This study explored NAC's impact on behavior in first and second-generation mice after SIS, focusing on HDAC2 and GCN5 expression in the hippocampus. Materials and methods: In this study, 24 male and 24 female mice were bred for one generation. The pups were divided into six (3male, 3female) groups (n = 20): 1- Control receiving normal saline, 2- SIS with normal saline, 3- SIS with NAC (150 mg/kg) IP for four weeks. Eight mice from each group underwent behavioral, histopathological, and molecular tests, while others were mated (4 males + 4 females) to produce second generations. These pups were divided into 9 groups (n = 8) for behavioral tests, including elevated plus maze, open field, forced swimming, and histopathological and molecular assessments (HDAC2 and GCN5 expression) in the hippocampus. Results: The SIS group showed increased HDAC2 and GCN5 expression. Following SIS, there was a decrease in open arm entries and passes in the open field test, alongside increased immobility in the forced swimming test and reduced CA1 and CA3 hippocampal diameters. NAC mitigated the adverse molecular, behavioral, and histopathological impacts of SIS across both generations. Conclusion: NAC reduces behavioral disorders after SIS (first and second generation) by reducing the expression of GCN5 and HDAC2 and increasing neuronal diameter in the hippocampus. Future research should investigate the long-term therapeutic effects of NAC for behavioral disorders after SIS.
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Registered trials
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