| Identification | Back Directory | [Name]
soyosaponin Ab | [CAS]
118194-13-1 | [Synonyms]
soyosaponin Ab
Soyasaponin Ab
Acetylsoyasaponin A1
Soyasaponin Ab
Acetylsoyasaponin A1
β-D-Glucopyranosiduronic acid, (3β,4β,21β,22β)-21,23-dihydroxy-22-[[3-O-(2,3,4,6-tetra-O-acetyl-β-D-glucopyranosyl)-α-L-arabinopyranosyl]oxy]olean-12-en-3-yl O-β-D-glucopyranosyl-(1→2)-O-β-D-galactopyranosyl-(1→2)- | [Molecular Formula]
C67H104O33 | [MDL Number]
MFCD28124367 | [MOL File]
118194-13-1.mol | [Molecular Weight]
1437.52 |
| Hazard Information | Back Directory | [Uses]
Soyosaponin Ab is a cytotoxic agent and acts as an immunomodulatory agent. | [in vivo]
Soyasaponin Ab (10-20 mg/kg; p.o.; daily for 5 days) shows inhibitory effect in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in male ICR mice[3].
Soyasaponin Ab (5-40 mg/kg; p.o.; one hour before the trial) significantly prevents Scopolamine (HY-N0296)-induced memory impairment in male ICR mice[4].
| Animal Model: | Male ICR mice (18-22 g, 5 weeks)[4] | | Dosage: | 5, 10, 20, 40 mg/kg | | Administration: | Oral gavage (p.o.); One hour before the trial, and memory impairment was induced by intraperitoneal injection of Scopolamine (0.9 mg/kg) 30 min after oral administrations of test agents. | | Result: | Restored memory impairment to 86% at a dose of 10 mg/kg of untreated normal control mice in the passive avoidance task.
Restored spontaneous alteration, which was lowered by Scopolamine on the Y-maze task.
Significantly shortened the escape latencies on the fifth day.
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| Animal Model: | Male institute of cancer research (ICR) mice (20-22 g, 4 weeks)[3] | | Dosage: | 10, 20 mg/kg | | Administration: | Oral gavage (p.o.); daily for 5 days | | Result: | Inhibited TNBS-induced body weight reduction, colon shortening, macroscopic score, and myeloperoxidase activity.
Inhibited the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
Ameliorated changes of TNBS-treated mouse colons which showed increased neutrophils, massive bowel edema, dense infiltration of the superficial layers of the mucosa, and epithelial cell disruption by large ulcerations.
Inhibited the expression of TLR4, COX-2, and iNOS and the phosphorylation of IRAK1, IKK-β and p65, although it reversed IRAK-1 expression.
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