“…jp/wiki/index.php/LCMS:Kangenkaryu) revealed paeoniflorin as one of the major chemical constituents of KK. There are also reports demonstrating that some chemical constituents from Salviae Miltiorrhizae Radix, tanshinone, and its congeners (43,44), such as rosmarinic acid (45,46) and lithospermate B (47), improve cognitive deficits caused by scopolamine, β-amyloid, or aging in rodents. However, the contribution of tanshinone and its congeners to the effect of KK seems to be limited or nonexistent, since their amounts included in the KK extract used in this study were low compared with those of paeoniflorin and other water-soluble constituents of KK.…”
Abstract.We investigated the effect of kangen-karyu (KK), a Chinese herbal prescription, on cognitive deficits and central cholinergic systems of type 2 diabetic db/db mice. Seven-week-old db/db (Y-db/db) mice received daily administration of test drugs during an experimental period of 12 weeks. At 18 weeks of age (O-db/db), the animals underwent the water maze test. Compared with age-matched control strain mice (O-m/m), vehicle-treated O-db/db mice showed impaired learning and memory performance. KK (100 -200 mg/kg per day) and the reference drug tacrine (THA: 2.5 mg/kg per day) ameliorated the performance of O-db/db mice without affecting their serum glucose level. O-db/db mice had lower levels of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the brain than O-m/m mice. Expression levels of central cholinergic marker proteins in the hippocampus and the number of cholinergic cells in the medial septum and basal forebrain were also significantly lower in O-db/db than in O-m/m mice, whereas no significant differences in the expression levels of these factors and the cell number were found between Y-m/m and Y-db/db mice. KK and THA treatment significantly reversed the down-regulated levels of cholinergic markers, choline acetyltransferase-positive cell number, and BDNF expression in db/db mice. These findings suggest that KK as well as THA prevents diabetes-induced cognitive deficits by attenuating dysfunction of central cholinergic systems.
“…jp/wiki/index.php/LCMS:Kangenkaryu) revealed paeoniflorin as one of the major chemical constituents of KK. There are also reports demonstrating that some chemical constituents from Salviae Miltiorrhizae Radix, tanshinone, and its congeners (43,44), such as rosmarinic acid (45,46) and lithospermate B (47), improve cognitive deficits caused by scopolamine, β-amyloid, or aging in rodents. However, the contribution of tanshinone and its congeners to the effect of KK seems to be limited or nonexistent, since their amounts included in the KK extract used in this study were low compared with those of paeoniflorin and other water-soluble constituents of KK.…”
Abstract.We investigated the effect of kangen-karyu (KK), a Chinese herbal prescription, on cognitive deficits and central cholinergic systems of type 2 diabetic db/db mice. Seven-week-old db/db (Y-db/db) mice received daily administration of test drugs during an experimental period of 12 weeks. At 18 weeks of age (O-db/db), the animals underwent the water maze test. Compared with age-matched control strain mice (O-m/m), vehicle-treated O-db/db mice showed impaired learning and memory performance. KK (100 -200 mg/kg per day) and the reference drug tacrine (THA: 2.5 mg/kg per day) ameliorated the performance of O-db/db mice without affecting their serum glucose level. O-db/db mice had lower levels of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the brain than O-m/m mice. Expression levels of central cholinergic marker proteins in the hippocampus and the number of cholinergic cells in the medial septum and basal forebrain were also significantly lower in O-db/db than in O-m/m mice, whereas no significant differences in the expression levels of these factors and the cell number were found between Y-m/m and Y-db/db mice. KK and THA treatment significantly reversed the down-regulated levels of cholinergic markers, choline acetyltransferase-positive cell number, and BDNF expression in db/db mice. These findings suggest that KK as well as THA prevents diabetes-induced cognitive deficits by attenuating dysfunction of central cholinergic systems.
“…1), isolated from S. miltiorrhiza, restored the diazepam (a GABA A /benzodiazepine receptor agonist) induced memory deficits in a passive avoidance test. This implied that tanshinone I or tanshinone II A prevented cholinergic dysfunction-related deterioration of learning and memory through the GABAergic neurotransmitter system [62]. Scutellaria baicalensis Georgi.…”
Section: Action Through Gabaergic Nervous Systemmentioning
confidence: 96%
“…Cryptotanshinone and 15,16-dihydrotanshinone I were proven to induce an inhibitory effect on AChE in in vitro and ex vivo studies. Tanshinone congeners may exert a beneficial effect on cognitive impairment by cholinergic signaling enhancement [62]. Salvia triloba L. f. (Lamiaceae): Its hydroalcoholic extract exerted a memory enhancing effect partially through AChE inhibition with an IC 50 value of 0.71 mg/mL.…”
“…Diazepam was administered in a dose of 1 mg/kg as this dose was found to produce cognitive decline (Kim et al 2007). EA was given in doses of 10, 30 and 100 mg/kg, 30 min before the administration of diazepam in the combination group.…”
(2016) Beneficial effects of ellagic acid against animal models of scopolamine-and diazepam-induced cognitive impairments, Pharmaceutical Biology, 54:10, 1947-1953, DOI: 10.3109/13880209.2015 PHARMACEUTICAL BIOLOGY, 2016 VOL. 54, NO. 10, 1947-1953 http://dx.doi.org/10.3109/13880209.2015 Context In a previous study, it has been shown that ellagic acid (EA), a polyphenolic compound found in pomegranate and different berries, prevents cognitive and hippocampal long-term potentiation (LTP) impairments induced by traumatic brain injury in rats through antioxidant and anti-inflammatory mechanisms.Objective The present study was conducted to assess the potential of EA as a memory enhancer.
Materials and methodsThe elevated plus maze (EPM) and passive avoidance (PA) paradigm were used to evaluate learning and memory parameters. Three doses (10, 30 and 100 mg/kg, i.p.) of EA were administered to animals. Memory impairment was induced by scopolamine treatment (0.4 mg/kg, i.p.) and/or diazepam (1 mg/kg, i.p.). Acquisition trials were carried out 30 min after scopolamine treatment and retention trials were performed for 5 min 24 h after the acquisition trials.Results EA at doses 30 and 100 mg/kg significantly reversed the amnesia induced by scopolamine (0.4 mg/kg, i.p.) in the EPM and PA tests in mice. Also, EA at doses 30 and 100 mg/kg significantly antagonized the amnesia induced by diazepam (1 mg/kg, i.p.) in EPM test in rats. Moreover, chronic administration of EA at dose 30 mg/kg ameliorated the memory deficit induced by diazepam (1 mg/ kg, i.p.) in rats. Discussion and conclusion This study demonstrates that ellagic acid is effective in preventing scopolamine-and diazepam-induced cognitive impairments without altering the animals' locomotion. This suggests the potential of EA application as a useful memory restorative agent in the treatment of dementia seen in elderly persons.ARTICLE HISTORY
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