Dataset Information

Time-Restricted Feeding Orchestrates Astrocytic Metabolic Reprogramming via the Wnt Pathway to Alleviate Sevoflurane-Induced Neural Injury

ABSTRACT:

Perioperative neurocognitive disorders (PND) pose a significant challenge for aging surgical patients, with sevoflurane anesthesia being an identified risk factor. Time-restricted feeding (TRF), a dietary regimen, shows promise in mitigating age-related cognitive decline, but its efficacy and mechanism against sevoflurane-induced PND remain unclear. Using the aging-accelerated mouse model (SAMP8) exposed to sevoflurane, we found that TRF improved cognitive performance and synaptic integrity, as evidenced by increased levels of PSD-95 and synaptophysin. Mechanistically, TRF activated the Wnt/β-catenin pathway, driving a beneficial metabolic reprogramming in hippocampal astrocytes characterized by enhanced ketogenesis and fatty acid oxidation. This was associated with reduced neuroinflammation and oxidative stress. The neuroprotective effects of TRF were abolished by Wnt inhibition and enhanced by Wnt activation. Our study identifies TRF as a non-pharmacological strategy that counteracts PND by linking Wnt-mediated astrocyte metabolic reprogramming to improved neuronal function.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS13891 | MetaboLights | 2026-02-17

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13891_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13891_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13891_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13891_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Age is the primary risk factor for many chronic diseases and cognitive decline during brain aging may increase dementia risk. Hallmarks of brain aging including neuronal dysfunction and glial contribute to reduced cognitive function, and there is a persistent lack of effective treatments. Bioactive plant compounds called “nutraceuticals” can target age-related cellular processes and may protect cognitive function. Apigenin is a flavone found in plants such as chamomile and can inhibit hallmarks of aging such as cellular senescence, mitochondrial dysfunction, and impaired proteostasis. However, the underlying mechanisms of apigenin in the brain are not fully understood. Here, we characterized brain transcriptome changes in young and old mice given apigenin in drinking water and examined potential mechanisms in human astrocytes. Consistent with previous studies, we observed improved novel object recognition in old mice treated with apigenin versus old controls. Transcriptome analyses in old controls found differentially expressed genes related to immune responses, inflammation, and cytokine regulation versus young. Fewer differences were observed in old apigenin-treated versus old controls, but these changes were related to development, behavior, and antiviral responses. The majority of upregulated genes in old mice were downregulated with apigenin treatment and associated with immune responses. Similarly, the genes that were reduced with aging, but increased in old apigenin-treated mice were related to pathways important for neurological function/disease, cellular maintenance, and homeostatic signaling. We also found that glial cells drove the majority of the transcriptome differences with aging and apigenin-treatment. To explore the mechanism of action for apigenin in glial cells, we treated replicatively aged astrocytes with apigenin and observed reduced markers of inflammation and cellular senescence. Collectively, our data support the role of apigenin as a protector of cognitive and neuronal function protectant through the suppression of neuroinflammatory genes and proteins and may be especially important in non-neuronal cells.

Dataset Information

Time-Restricted Feeding Orchestrates Astrocytic Metabolic Reprogramming via the Wnt Pathway to Alleviate Sevoflurane-Induced Neural Injury

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