liriodendrin--1r-(1alpha-3abeta-4beta-6aalpha)-isomer and Cognitive-Dysfunction

liriodendrin--1r-(1alpha-3abeta-4beta-6aalpha)-isomer has been researched along with Cognitive-Dysfunction* in 2 studies

Other Studies

2 other study(ies) available for liriodendrin--1r-(1alpha-3abeta-4beta-6aalpha)-isomer and Cognitive-Dysfunction

ArticleYear
Eleutheroside E supplementation prevents radiation-induced cognitive impairment and activates PKA signaling via gut microbiota.
    Communications biology, 2022, 07-08, Volume: 5, Issue:1

    Topics: Animals; Cognitive Dysfunction; Dietary Supplements; Gastrointestinal Microbiome; Glucosides; Lignans; Mice

2022
Eleutheroside E attenuates isoflurane-induced cognitive dysfunction by regulating the α7-nAChR-NMDAR pathway.
    Neuroreport, 2019, 02-06, Volume: 30, Issue:3

    There is growing evidence that cognitive dysfunction induced by anesthetics is adversely affecting a large number of elderly surgical patients. Eleutheroside E (EE), a principal component of Eleutherococcus senticosus, exerts obvious protective effects on cognition. The aim of this study was to investigate the neuroprotective effect of EE on isoflurane (ISO)-induced cognitive dysfunction and explore the possible mechanisms. Learning and memory are assessed in novel object recognition and Morris water maze. We found that with ISO exposure, aged rats had a lower preference for the new object and spent less time in the target quarter. However, the amnesia can be alleviated by EE (50 mg/kg, intraperitoneally). Further research focused on the possible protective molecules associated with learning and memory, such as acetylcholine (ACh) and choline acetyltransferase (ChAT), nicotinic acetylcholine receptors (α7-nAChR), and NR2B, is required. The ACh in the hippocampus and serum was decreased after ISO exposure; meanwhile, the expression of ChAT, α7-nAChRs, and NR2B was downregulated. This abnormal state can be reversed by the administration of EE. Here, our results suggested that EE may be a potential therapeutic agent against ISO-induced cognitive dysfunction. The possible mechanism can be attributed to its neuroprotection through enhancing ChAT, which promotes the synthesis of ACh, further influencing the expression of the α7-nAChR-NR2B complex.

    Topics: Acetylcholine; Animals; Cognition; Cognitive Dysfunction; Glucosides; Hippocampus; Isoflurane; Lignans; Male; Memory; Neuroprotective Agents; Nicotinic Agonists; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Receptors, Nicotinic

2019