ArticleChinese medicine2025
Buyang Huanwu Decoction improves energy metabolism disorders after cerebral ischemia-reperfusion by regulating the SIRT1/AMPK signaling pathway to promote glycolysis and the tricarboxylic acid cycle.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives.Journal of cellular and molecular medicine · 2026Review
- Protective effect and mechanisms of Buyang Huanwu decoction against hypobaric hypoxia-induced brain injury in mice: involvement of inflammatory responses and HIF-1/PI3K-Akt-related pathways.Frontiers in immunology · 2026Article
- Neuroprotective mechanisms of Buyang Huanwu decoction in ischemic stroke.Frontiers in pharmacology · 2025Review
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9 authors.
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Abstract
backgroundBuyang Huanwu Decoction (BYHWD), a traditional Chinese medicine formula for cerebral infarction, exerts neuroprotective effects by enhancing cerebral energy metabolism, yet its precise mechanisms remain elusive.
objectiveTo explore the effects of BYHWD on improving cerebral ischemia-reperfusion injury (CIRI) with Qi deficiency and blood stasis syndrome from an energy metabolism perspective and verify it through experiments.
methodsA rat model of CIRI with Qi deficiency and blood stasis syndrome was established and intervened with BYHWD. The therapeutic effect of BYHWD was evaluated using Longa score, Qi deficiency and blood stasis syndrome score, pathological staining, and colorimetric assays. Untargeted metabolomics was used to identify differential metabolites and regulatory mechanisms, and in vivo and in vitro models were constructed for validation.
resultsBYHWD ameliorated neurological deficits and Qi deficiency and blood stasis syndrome in rats, reduced brain pathology, and increased energy substances. Untargeted metabolomics analysis suggested BYHWD enhanced cerebral energy metabolism via nicotinate and nicotinamide metabolism and AMPK signaling, involving SIRT1/AMPK regulation and promotion of glycolysis and the tricarboxylic acid (TCA) cycle. Validation experiments showed BYHWD activated the SIRT1/AMPK signaling pathway in brain tissue, promoting glucose uptake and enhancing the expression of proteins related to glycolysis, mitochondrial biogenesis, and the TCA cycle. Similar results were observed in HT22 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R).
conclusionBYHWD improved cerebral energy metabolic disorders by activating the SIRT1/AMPK signaling pathway, thereby enhancing glycolytic capacity and TCA cycle capacity. This study elucidated the mechanisms of BYHWD and provided a theoretical basis for its rational application.
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