1. MAPK/ERK Pathway Stem Cell/Wnt Epigenetics Neuronal Signaling Protein Tyrosine Kinase/RTK
  2. ERK Epigenetic Reader Domain Trk Receptor
  3. Polygalasaponin XXXII

Polygalasaponin XXXII is an orally active cognitive enhancer. Polygalasaponin XXXII promotes the phosphorylation of ERK, CREB, Synapsin I and TrkB. Polygalasaponin XXXII enhances basal synaptic transmission. Polygalasaponin XXXII attenuates Scopolamine (HY-N0296)-induced cognitive impairment and improves hippocampus-dependent learning and memory abilities. Polygalasaponin XXXII can be used in research related to cognitive dysfunction.

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Polygalasaponin XXXII

Polygalasaponin XXXII Chemical Structure

CAS No. : 176182-04-0

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Description

Polygalasaponin XXXII is an orally active cognitive enhancer. Polygalasaponin XXXII promotes the phosphorylation of ERK, CREB, Synapsin I and TrkB. Polygalasaponin XXXII enhances basal synaptic transmission. Polygalasaponin XXXII attenuates Scopolamine (HY-N0296)-induced cognitive impairment and improves hippocampus-dependent learning and memory abilities. Polygalasaponin XXXII can be used in research related to cognitive dysfunction[1][2][3].

IC50 & Target[1]

TrkB

 

In Vitro

Polygalasaponin XXXII (1 μM; 4 min) rapidly activates phosphorylation of ERK, CREB, and synapsin I in primary rat hippocampal neurons (5 DIV)[1].
Polygalasaponin XXXII protects PC12 cells against serum deficiency-induced damage[3].
Polygalasaponin XXXII protects PC12 cells against Glutamate (HY-W250122)-induced neurotoxicity[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Polygalasaponin XXXII (0.125-2 mg/kg; p.o.; once daily; for 16 consecutive days) significantly improves scopolamine (HY-N0296)-induced cognitive impairment in mice, with the 2 mg/kg dose exerting the most prominent molecular and behavioral effects[1].
Polygalasaponin XXXII (400 μM; intracerebroventricular injection; single administration) significantly enhances basal synaptic transmission in the dentate gyrus of anesthetized rats and induces long-term potentiation[1].
Polygalasaponin XXXII (0.125-2 mg/kg; p.o.; once daily; for 19 consecutive days) improves scopolamine (HY-N0296)-induced cognitive impairment in mice, and the 0.5 mg/kg and 2 mg/kg doses significantly enhance the phosphorylation level of TrkB in the hippocampus[3].
Polygalasaponin XXXII (5 μL of 400 μM solution; intracerebroventricular injection; single administration) significantly enhances hippocampal LTP in rats, with its PS amplitude reaching up to 378% of the baseline level[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (male, 8 weeks old, 18-20 g, scopolamine-induced amnesia)[1]
Dosage: 0.125 mg/kg; 0.5 mg/kg; 2 mg/kg
Administration: p.o.; daily; 16 days
Result: Increased swimming time in the target quadrant during probe trial significantly compared to scopolamine model group.
Shortened scopolamine-prolonged escape latency significantly at 0.125 mg/kg and 2 mg/kg doses; showed a trend toward shorter latency at 0.5 mg/kg dose (P=0.053).
Increased hippocampal ERK phosphorylation significantly compared to both control and model groups at all doses.
Increased hippocampal CREB phosphorylation significantly compared to both control and model groups at 0.5 mg/kg and 2 mg/kg doses; significantly increased CREB phosphorylation compared to model group at 0.125 mg/kg dose.
Reversed scopolamine-induced attenuation of synapsin I phosphorylation significantly at 2 mg/kg dose.
Increased hippocampal BDNF levels significantly compared to model group at all doses; increased BDNF levels compared to control group at 2 mg/kg dose.
Animal Model: Wistar (male, 3 months old, 230-260 g)[1]
Dosage: 1 μmol/L
Administration: i.c.v.; single dose
Result: Increased population spike amplitude to 162% of baseline within 5 min of administration.
Reached population spike amplitudes of 172%, 215%, and 254% of baseline at 10, 30, and 60 min post-administration, respectively.
Induced long-term potentiation in the hippocampal dentate gyrus, as shown by sustained increase of over 30% above baseline for more than 30 min.
Animal Model: C57BL/6J (male, 18-20 g)[3]
Dosage: 5 mg/kg·d-1; 20 mg/kg·d-1
Administration: p.o.; daily; 13 days
Result: Significantly reversed scopolamine-induced increases in channel water maze latency time and error numbers (5 mg/kg dose only).
Demonstrated no significant efficacy relative to the model group (20 mg/kg dose only).
Animal Model: Wistar (male, 3 months old, 230-260 g)[3]
Dosage: 5 μL of 400 μmol/L solution (final brain concentration of 1 μmol/L)
Administration: i.c.v.; single injection
Result: Significantly enhanced HFS-induced LTP compared to the control group.
Increased population spike (PS) amplitudes to 310% within 20 minutes post-injection, and reached 340%, 378%, and 366% at 40, 50, and 55 minutes post-injection, respectively.
Molecular Weight

1675.76

Formula

C79H118O38

CAS No.
SMILES

OC[C@](C([C@]1([H])CC2(C)C)=CC[C@]3([H])[C@]4(C[C@@H]5O)C)(CC[C@]1(CC2)C(O[C@H](O[C@@H]6C)[C@@H]([C@H]([C@H]6OC(/C=C/C(C=C7)=CC=C7OC)=O)O[C@H](O[C@H]8C)[C@@H]([C@@H]([C@H]8O)O)O)O[C@H](O[C@H]9C)[C@@H]([C@@H]([C@H]9O[C@H](OC[C@H]%10O)[C@@H]([C@H]%10O[C@H](OC[C@@H]%11O)[C@@H]([C@H]%11O)O)O)O[C@H](OC[C@](O)%12CO)[C@@H]%12O)O)=O)[C@@]3(CC[C@@]4([H])[C@@](C)([C@H]5O[C@@H]([C@@H]([C@H]%13O)O)O[C@@H]([C@H]%13O)CO)C(O)=O)C

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Polygalasaponin XXXII
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