ArticleCNS neuroscience & therapeutics2017
Pseudoginsenoside-F11 attenuates cerebral ischemic injury by alleviating autophagic/lysosomal defects.
Article in CNS neuroscience & therapeutics, 2017. 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, 41 citations in OpenAlex.
- M2 microglial exosomal miR-1949 ameliorates sepsis-associated encephalopathy through DKK1/Wnt/β-catenin-mediated microglial repolarization.Archives of pharmacal research · 2026Article
- Pseudoginsenoside-F11: a comprehensive review of chemical structure, pharmacological activities, pharmacokinetics, and therapeutic potential.Frontiers in pharmacology · 2026Review
- Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.Biology · 2025Review
- Neuroprotective effects of phytochemicals through autophagy modulation in ischemic stroke.Inflammopharmacology · 2025Review
- Exosomes: an innovative therapeutic target for cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- The Pathological Mechanism of Neuronal Autophagy-Lysosome Dysfunction After Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- Melibiose Confers a Neuroprotection against Cerebral Ischemia/Reperfusion Injury by Ameliorating Autophagy Flux via Facilitation of TFEB Nuclear Translocation in Neurons.Life (Basel, Switzerland) · 2021Article
- Pseudoginsenoside-F11 attenuates cognitive dysfunction and tau phosphorylation in sporadic Alzheimer's disease rat model.Acta pharmacologica Sinica · 2021Article
- Pseudoginsenoside F11 Enhances the Viability of Random-Pattern Skin Flaps by Promoting TFEB Nuclear Translocation Through AMPK-mTOR Signal Pathway.Frontiers in pharmacology · 2021Article
- Neuroprotective Phytochemicals in Experimental Ischemic Stroke: Mechanisms and Potential Clinical Applications.Oxidative medicine and cellular longevity · 2021Review
- Decreased neuronal synaptosome associated protein 29 contributes to poststroke cognitive impairment by disrupting presynaptic maintenance.Theranostics · 2021Article
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- Pseudoginsenoside-F11 Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Neutrophil Infiltration and Accelerating Neutrophil Clearance.Inflammation · 2019Article
- Urolithin A-activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo.CNS neuroscience & therapeutics · 2019Article
- American Ginseng (Nutrients · 2019Review
- Neuronal-targeted TFEB rescues dysfunction of the autophagy-lysosomal pathway and alleviates ischemic injury in permanent cerebral ischemia.Autophagy · 2019Article
- The role of autophagy in acute brain injury: A state of flux?Neurobiology of disease · 2019Review
- Active ginseng components in cognitive impairment: Therapeutic potential and prospects for delivery and clinical study.Oncotarget · 2018Review
- Pseudoginsenoside-F11 attenuates cerebral ischemic injury by alleviating autophagic/lysosomal defects.CNS neuroscience & therapeutics · 2017Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been reported to exert wide-ranging neuroprotective properties. The aim of this study was to investigate the effect and potential mechanisms of PF11 on the autophagic/lysosomal pathway following ischemic stroke.
methodsMale Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO). Cerebral ischemia outcome, TUNEL staining, Fluoro-Jade B staining were carried out 24 hours poststroke. The autophagic/lysosomal-related proteins were measured.
resultsA single administration of PF11 significantly decreased the infarct area, reduced the brain water content, and improved neurological functions, even 4 hours after the onset of pMCAO. Meanwhile, PF11 lessened the ischemic insult-mediated loss of neurons and activation of astrocytes and microglia. Furthermore, PF11 attenuated pMCAO-induced accumulations of autophagosomes and apoptosis. We further observed a remarkable effect of PF11 in reversing the ischemic insult-induced accumulation of autophagosomes (LC3-II) and abnormal aggregation of autophagic proteins (SQSTM1 and ubiquitin). Furthermore, PF11 was capable of improving lysosomal function and lysosome/autophagosome fusion following pMCAO, and this change was reversed by the lysosomal inhibitor chloroquine. Also, the improvement of ischemic outcome and the antiapoptotic effect induced by PF11 was reversed by CQ.
conclusionThese findings indicate that the autophagic flux is impaired in a rat model of pMCAO, and that PF11 exerts an excellent protective effect against ischemic stroke by alleviating autophagic/lysosomal defects.
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