ArticleCell stress & chaperones2023
Aucubin promotes activation of AMPK and alleviates cerebral ischemia/reperfusion injury in rats.
Article in Cell stress & chaperones, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Iridoids as Multi-target Neuroprotective Agents for Ischemic Stroke: Mechanisms and Therapeutic Potential.Mini reviews in medicinal chemistry · 2026Review
- Propofol Modulates Microglial Glucose Metabolism Via the AMPK/HIF-1α Signaling Pathway To Ameliorate ECS-induced Cognitive Deficits in Depressive-like Rats.Neurochemical research · 2025Article
- Protective Role of Oxycodone in Myocardial Oxidative Stress and Mitochondrial Dysfunction Induced by Ischemia-Reperfusion.Journal of biochemical and molecular toxicology · 2025Article
- Aucubin Alleviates Chronic Obstructive Pulmonary Disease by Activating Nrf2/HO-1 Signaling Pathway.Cell biochemistry and biophysics · 2024Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the current investigation, we explored the benefits of aucubin against rodent ischemia/reperfusion (I/R) damages in brains and elucidated the role of 5'-AMP-activated protein kinase (AMPK) in its neuroprotective action. I/R model of brain was established in male three-month-old rats through 2 h of middle cerebral artery occlusion followed by two days of reperfusion. Aucubin boosted phosphorylation of AMPKα in ipsilateral cortex of injured rats. Then, rats were exposed to cerebral I/R damage and received treatment of aucubin and compound C (a well-known AMPK inhibitor). It was found that aucubin administration improved neurological symptom score, decreased infarct volume, and mitigated cerebral edema in injured rats. Aucubin administration upregulated Nrf2 expression and abated oxidative stress in ipsilateral cortex of injured rats. Aucubin administration reduced levels of multiple pro-inflammatory cytokines, suppressed microglial activation and neutrophil infiltration, and promoted M2 polarization in injured rats. More importantly, compound C abolished the neuroprotective, anti-oxidant and inflammation-modulating effects of aucubin in injured rats, at least in part. Therefore, we concluded that activation of AMPK by aucubin alleviated I/R injury in brain through abating oxidative stress and suppressing inflammation, identifying a potential candidate for those patients of ischemic stroke.
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