ArticleJournal of cellular and molecular medicine2025
Berberine Ameliorates Postoperative Cognitive Dysfunction in Aged Mice and Regulates the PI3K-AKT Pathway: A Network Pharmacology Study.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- Berberine Ameliorates Postoperative Cognitive Dysfunction in Aged Mice and Regulates the PI3K-AKT Pathway: A Network Pharmacology Study.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
In this study, we investigated the therapeutic potential of Berberine (BBR), an anti-inflammatory agent capable of penetrating the blood-brain barrier, for mitigating postoperative cognitive dysfunction (POCD) in aged mice. BBR was administered at a dose of 10 mg/kg daily for 2 weeks and significantly improved cognitive impairments induced by surgical and anaesthesia-related factors. Specifically, BBR markedly suppressed glial cell activation and reduced levels of pro-inflammatory cytokines such as tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β). Additionally, it alleviated oxidative stress markers and lipid accumulation. Using network pharmacology analysis, we demonstrated that BBR modulates neuroinflammation, oxidative processes and lipid metabolism by inhibiting the phosphorylation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway. Furthermore, extended research revealed that BBR upregulated the expression of PPAR-γ mRNA, suggesting a neuroprotective mechanism via regulation of the PI3K-Akt pathway. These findings support the potential application of BBR as a therapeutic agent for managing POCD in elderly populations.
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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 Socratic graph.