ArticleFrontiers in pharmacology2025
Gypenoside XLIX inhibiting PI3K/AKT/FOXO1 signaling pathway mediated neuronal mitochondrial autophagy to improve patients with ischemic stroke.
Article in Frontiers in pharmacology, 2025. 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.
- The Protective Mechanism of Continuous Theta Burst Stimulation in the Acute Phase of Stroke Through Modulation of the Calcineurin/AKT/FOXO1 Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- Gypenoside XLIX and Mitochondria-Associated ER Membranes in Non-Alcoholic Fatty Liver Disease: Mechanistic Insights and Emerging Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Gypenosides attenuate HAmerican journal of translational research · 2026Article
- Exploring the Anti-Inflammatory Activity of the Heat-ProcessedInternational journal of molecular sciences · 2025Article
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10 authors.
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Abstract
Introduction: Ischemic stroke is a leading cause of mortality and disability worldwide, with limited therapeutic options and high rates of recurrence. Mitochondrial dysfunction plays a critical role in neuronal injury during ischemia-reperfusion, making mitochondrial autophagy a potential therapeutic target. Gypenoside XLIX, a major active metabolite of Gynostemma pentaphyllum, exhibits antioxidant and organ-protective properties, but its effects on neuronal mitochondrial damage in stroke remain unclear. This study aimed to explore the neuroprotective mechanisms of Gypenoside XLIX in ischemic stroke, focusing on the PI3K/AKT/FOXO1 signaling pathway. Methods: Neuroprotective effects were evaluated in oxygen-glucose deprivation (OGD) neuronal cells and middle cerebral artery occlusion (MCAO) rat models. Cell viability, apoptosis, ROS production, mitochondrial membrane potential, and autophagic flux were assessed by CCK-8, flow cytometry, ELISA, TMRE staining, immunofluorescence, and Western blotting. Signaling pathway involvement was examined using PI3K inhibitor LY294002, AKT activator SC79, and FOXO1 knockdown. Results: Gypenoside XLIX significantly improved neuronal viability (p < 0.01), reduced apoptosis (p < 0.01), and decreased ROS levels (p < 0.001) in OGD cells. It enhanced p-PI3K and p-AKT expression while suppressing FOXO1 (p < 0.05), promoted Beclin-1, LC3, PINK1, and Parkin expression (p < 0.001), and reduced p62 (p < 0 .01). In MCAO rats, Gypenoside XLIX decreased infarct volume (p < 0.001), brain edema (p < 0.01), and TUNEL-positive cells (p < 0.001), while elevating mitochondrial membrane potential and antioxidant enzyme levels (SOD, GSH-Px, CAT; all p < 0.001). Conclusion: Gypenoside XLIX alleviates ischemic stroke injury by activating the PI3K/AKT/FOXO1 pathway, enhancing mitochondrial autophagy, and reducing oxidative stress, supporting its potential as a novel neuroprotective agent in stroke management.
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