ArticleCytoJournal2025
Nobiletin alleviates brain injury in uremic mice and inhibits indoxyl sulfate-induced neurotoxicity in HT22 cells through the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Uremic encephalopathy presents as central nervous system symptoms in acute and chronic renal failure. Nobiletin (NOB), an extract from chenpi, has demonstrated anti-inflammatory bioactivity and potential neuroprotective effects without remarkable toxicity. This study aims to evaluate the pharmacological effects of NOB on treating uremic brain injury and elucidate its underlying mechanisms. Material and Methods: A uremic encephalopathy mouse model was established by inducing renal failure with cisplatin (DDP). The therapeutic effects of NOB were investigated by assessing its effect on brain damage and neuronal viability. HT22 murine hippocampal neurons were also treated with DDP to induce neurotoxicity, and the effects of NOB on cell viability, apoptosis, and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway were examined. The PI3K inhibitor LY294002 was used to further investigate the involvement of the PI3K/Akt pathway in the neuroprotective effects of NOB. Results: NOB alleviated uremia-induced brain damage in mice, and this function was associated with the activation of the PI3K/Akt signaling pathway. Conclusion: NOB exerts potent neuroprotective effects by activating the PI3K/Akt pathway, mitigating uremia-induced brain injury and preventing DDP-induced neurotoxicity. These findings support the potential therapeutic application of NOB for uremic encephalopathy and provide insights into its underlying mechanisms.
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