ArticleJournal of neuroinflammation2022
Neuroprotective effects of alisol A 24-acetate on cerebral ischaemia-reperfusion injury are mediated by regulating the PI3K/AKT pathway.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- CORM-2 protects against sepsis-associated encephalopathy by activating the Nrf2/SLC7A11/GPX4 axis to inhibit ferroptosis and neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Alisols A-C and their acetate derivatives: a review of natural occurrence, pharmacology, semisynthesis, pharmacokinetics, and metabolism.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Astragaloside IV suppresses neuroinflammation via PI3K/Akt/NF-κB to ameliorate cerebral ischemia-reperfusion injury based on network pharmacology analysis and experimental validation.Frontiers in immunology · 2026Article
- Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026Review
- Noninvasive method for achieving the regeneration of damaged nerves via ultrasonic nasal drops.Bioactive materials · 2025Article
- Entrectinib can induce nerve cell damage by inhibiting PI3K-AKT and TGF-β signaling pathways.Frontiers in pharmacology · 2025Article
- Mechanism of Efferocytosis in Determining Ischaemic Stroke Resolution-Diving into Microglia/Macrophage Functions and Therapeutic Modality.Molecular neurobiology · 2024Review
- Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy.Molecular neurobiology · 2024Review
- TXNIP/NLRP3 aggravates global cerebral ischemia-reperfusion injury-induced cognitive decline in mice.Heliyon · 2024Article
- Alisol A, the Eye-Entering Ingredient ofDrug design, development and therapy · 2024Article
- Article
- ChemR23 activation attenuates cognitive impairment in chronic cerebral hypoperfusion by inhibiting NLRP3 inflammasome-induced neuronal pyroptosis.Cell death & disease · 2023Article
- Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway.Aging · 2023Article
- Mechanism of Resveratrol Improving Ischemia-Reperfusion Injury by Regulating Microglial Function Through microRNA-450b-5p/KEAP1/Nrf2 Pathway.Molecular biotechnology · 2023Article
- Alisol A 24-acetate ameliorates osteoarthritis progression by inhibiting reactive oxygen species and inflammatory response through the AMPK/mTOR pathway.Immunity, inflammation and disease · 2023Article
- Review
- Terpenoid natural products exert neuroprotectionFrontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeuroinflammation and apoptosis are involved in the pathogenesis of ischaemic stroke. Alisol A 24-acetate (24A) exerts a strong inhibitory effect on inflammation and cell apoptosis. The neuroprotective effect of 24A on global cerebral ischaemia/reperfusion (GCI/R) injury remains unclear.
methodsGCI/R mice were used to investigate the neuroprotective effect of 24A. Modified neurological deficit scores, Morris water maze and object recognition tests were used to evaluate behaviours. Metabolism in brain regions was detected using magnetic resonance spectroscopy (MRS), and changes in microglia, astrocytes and neurons were detected. Inflammation and apoptosis were measured.
resultsThe results showed that 24A suppressed neurological deficits scores and improved GCI/R induced cognitive dysfunction. It was also observed that 24A could alleviate neuroinflammation, which manifested as 24A inhibited microglia and astrocytes proliferation, downregulated the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and inducible nitric oxide synthase (iNOS) in the GCI/R mice brain. The apoptosis of neurons reduced, and dendritic spines of hippocampal neurons increased in the presence of 24A. In addition, 24A could up-regulate the expression of phosphorylated phosphoinositide 3-kinases (p-PI3K) and phosphorylated protein kinase B (p-AKT) in GCI/R mice brain, and all the morphological, neurological, and biochemical changes of 24A treatment were abolished by the application of PI3K/AKT pathway inhibitor LY294002.
conclusionsTaken together, our study indicated that 24A alleviated GCI/R injury by inhibiting neuroinflammation and apoptosis through the regulation of the PI3K/AKT pathway.
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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.