Pseudoginsenoside F11

Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of Aβ_1-40, downregulates the expression of JNK2, p53 and activated Caspase 3, and restores the activities of SOD and Glutathione peroxidase. Pseudoginsenoside F11 inhibits the excessive activation of μ-Calpain and restores the level of neuronal Nitric oxide synthase. Pseudoginsenoside F11 reduces infarct volume, alleviates cerebral edema, decreases neuronal loss, improves neurological deficits and enhances long-term functional outcomes in transient cerebral ischemia models. Pseudoginsenoside F11 antagonizes Methamphetamine-induced behavioral deficits, dopamine level reduction and neurotoxicity without altering the baseline behaviors of normal mice. Pseudoginsenoside F11 can be used in studies related to Alzheimer's disease, transient cerebral ischemic injury and Methamphetamine-induced neurotoxicity^[1][2][3]. In Vitro:Pseudoginsenoside F11 (10-100 μM; 2 h pre-treatment; 0-24 h OGD/R) protects cultured primary cortical neurons against OGD/R-induced injury by increasing cell viability, restoring neurite structure, maintaining calcium homeostasis, replenishing ATP levels, inhibiting μ-Calpain-mediated α-Fodrin cleavage, reversing deficits in NMDA receptor subunits/PSD95/nNOS, and alleviating endoplasmic reticulum stress, with the most robust effects observed at 100 μM^[2]. In Vivo:Pseudoginsenoside F11 (0.32-8 mg/kg; p.o.; daily; 15 days) significantly mitigates Aβ₁-4₂-induced learning and memory impairment in KM mice, with the 8 mg/kg dose showing robust improvement across both Morris water maze and step-through tests^[1].
Pseudoginsenoside F11 (8 mg/kg; p.o.; daily; 28 days) significantly improves learning and memory deficits in APP/PS1 mice, mediated by reduced amyloidogenesis, restored antioxidant function, reduced neuronal apoptosis, and improved neuronal histopathology^[1].
Pseudoginsenoside F11 (12 mg/kg; i.v.; single dose, 0-8 hours post-reperfusion; 3-12 mg/kg; i.v. initial dose, i.p. daily; 14 days) produces dose-dependent neuroprotection in transient cerebral ischemia-reperfusion injured rats, reducing acute brain damage by up to 48.1% infarct volume reduction with a 4-hour therapeutic window, improving long-term survival by 13.6% at 12 mg/kg, and restoring motor function and neuronal health via repression of sustained calcium overload^[2].
Pseudoginsenoside F11 (4-8 mg/kg; p.o.; two times at 4-hour intervals) significantly protects against methamphetamine-induced behavioral neurotoxicities (anxiety, despair, memory impairment) and partially reverses methamphetamine-induced brain dopamine depletion in mice^[3].