Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.1.7 (
acetylcholinesterase
)
28,390
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Anemarrhena asphodeloides Bunge (AA, family Liliaceae), which primarily contains xantones, such as mangiferin, and steroidal saponins, such as timosaponin AIII and sarsasapogenin, has been used as an anti-pyretic, anti-inflammatory, anti-diabetic, anti-platelet aggregation, and anti-depressant agent in traditional Chinese medicine. In the present study, the memory-enhancing effects of these saponins were investigated in scopolamine-treated mice. Among saponins, timosaponin AIII (
TA3
) significantly reversed the scopolamine-induced deficits in a passive avoidance test and in the Morris water maze test.
TA3
also increased hippocampal acetylcholine levels in scopolamine-treated mice and dose-dependently inhibited
acetylcholinesterase
(
AChE
) activity (IC(50) value, 35.4 microM). When
TA3
(50 mg/kg) was orally administered to mice and its blood concentration was measured by liquid chromatography and tandem mass spectrometry, the C(max) of
TA3
occurred 4-6 h after
TA3
treatment. The memory-enhancing effect of
TA3
was greater when it was administered 5 h before the acquisition trial than 1 h before. Scopolamine treatment in mice increased brain levels of TNF-alpha and IL-1beta expression. However, treatment with
TA3
and scopolamine inhibited the increase of TNF-alpha and IL-1beta expression. These results suggest that scopolamine may cause learning and memory deficits that are further complicated by inflammation.
TA3
also inhibited the activation of NF-kappaB signaling in BV-2 microglia and in SK-N-SH neuroblastoma cells induced with TNF-alpha or scopolamine. Nevertheless,
TA3
may ameliorate memory deficits, mainly by inhibiting
AChE
.
...
PMID:Timosaponin AIII, a saponin isolated from Anemarrhena asphodeloides, ameliorates learning and memory deficits in mice. 1942 56