• Journal of Physiology & Pathology in Korean Medicine
• /
• v.24 no.2
• /
• pp.228-235
• /
• 2010

This study was performed to investigate the memory enhancing effect of Poria cocos Wolf (Hoelen cum radix) against scopolamine-induced amnesia in Sprague-Dawley (SD) rats. To induce amnesia, scopolamine (0.75 mg/kg) was intraperitonically injected into SD rats 30 min before starting behavior tests. We have conducted Morris water-maze and Y-maze tests to monitor learning and memory functions. Poria cocos effectively reversed scopolamine-induced memory impairment in SD rats which was represented by an improvement of mean escape latency in water-maze test and spontaneous alterations in Y-maze test. To elucidate possible molecule mechanism, we have measured mRNA as well as protein expression of acetylcholine esterase (AchE), choline acetyltransferase (ChAT), muscarinic acetylcholine receptor (mAchR), and brain-derived neurotrophic factor (BDNF) using RT-PCR and Western blot analysis, respectively. Poria cocos increased mRNA levels of ChAT and mAchR in rat hippocampus compared with those in the scopolamine-injected amnesic group. In addition, protein expression of ChAT and BDNF was also elevated by Poria cocos intake. Furthermore, as an upstrem regulator, the activation of cAMP response element-binding protein (CREB) was assessed by immunohistochemistry. In this immunohistochemical analysis, the phosphorylation of CREB (p-CREB) was reduced by scopolamine injection, which was restored back to control levels by administration of Poria cocos. These results suggest that Poria cocos may improve memory and cognitive deficit in amnesia and have therapeutic potentials through up-regulation of ChAT, mAchR, and BDNF, which seemed to be mediated by activation of CREB.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.42 no.8
• /
• pp.1190-1196
• /
• 2013

The purpose of this study was to investigate the mechanism and effects of different types of ginseng on memory improvement in an experimental rat model. In this study, SD rats were induced for memory deficits through scopolamine treatment (1 mg/kg, i.p.) then administrated with ginseng extract for 7 weeks. The rats were divided into five groups: saline (1 mL/kg, NC: negative control), white ginseng (300 mg/kg, WG), red ginseng (300 mg/kg, RG), black ginseng (300 mg/kg, BG), and scopolamine (1 mg/kg, PC: positive control). The step through latency of the BG and RG groups was significantly longer than the PC group in the retention trial of multiple trial passive avoidance test. In the spatial reference memory triads of the Morris water maze test, the latency time of BG and RG was significantly lower than the PC group. In addition, in the prove test, the time spent in the platform quadrant of BG and RG groups were significantly longer than the PC group. Brain choline acetyltransferase (ChAT) activities BG and RG groups significantly increased compared to other groups. On the other hand, the levels of malondialdehyde (MDA) were significantly lower in the BG and RG groups compared to other groups. These result suggested that black ginseng could be useful to enhance learning memory and cognitive function by regulation of cholinergic enzymes.

• Biomolecules & Therapeutics
• /
• v.22 no.3
• /
• pp.176-183
• /
• 2014

Cognitive impairment is a result of dementia of diverse causes, such as cholinergic dysfunction and Alzheimer's disease (AD). Houttuynia cordata Thunb. (Saururaceae) has long been used as a traditional herbal medicine. It has biological activities including protective effects against amyloid beta ($A{\beta}$) toxicity, via regulation of calcium homeostasis, in rat hippocampal cells. To extend previous reports, we investigated the effects of water extracts of H. cordata herb (HCW) on tauopathies, also involving calcium influx. We then confirmed the effects of HCW in improving memory impairment and neuronal damage in mice with Ab-induced neurotoxicity. We also investigated the effects of HCW against scopolamine-induced cholinergic dysfunction in mice. In primary neuronal cells, HCW inhibited the phosphorylation of tau by regulating p25/p35 expression in $A{\beta}$-induced neurotoxicity. In mice with $A{\beta}$-induced neurotoxicity, HCW improved cognitive impairment, as assessed with behavioral tasks, such as novel object recognition, Y-maze, and passive avoidance tasks. HCW also inhibited the degeneration of neurons in the CA3 region of the hippocampus in Ab-induced neurotoxicity. Moreover, HCW, which had an $IC_{50}$ value of $79.7{\mu}g/ml$ for acetylcholinesterase inhibition, ameliorated scopolamine-induced cognitive impairment significantly in Y-maze and passive avoidance tasks. These results indicate that HCW improved cognitive impairment, due to cholinergic dysfunction, with inhibitory effects against tauopathies and cholinergic antagonists, suggesting that HCW may be an interesting candidate to investigate for the treatment of AD.

• The Journal of Korean Physical Therapy
• /
• v.26 no.6
• /
• pp.436-441
• /
• 2014

Purpose: The objective of this study was to offer clinical primary data that it's aims to examine effects of transcranial direct current stimulation (tDCS) on cognitive function and biochemical change of rat with alzheimer's disease(AD) induced by injecting scopolamine. Methods: Subjects were instructed cognitive dysfunction model, rat of Sprague-Dawley system was injected with scopolamine and each experimental group was classified into three; group I (n=16) is non-treatment groups; group II (n=16) is applied with the tacrine; group III (n=16) is applied with the tDCS. The ziggurat task test was conducted to observe behavioral changes and cognitive function ability and 7, 14, 21, 28 days after the model. Acetylcholine Esterase (Ach E) activity was examined for biochemical assessment of which the results are followed. Results: Participants showed as to behavioral change, tacrine application group was the most significantly responded, following tDCS application group. As to biochemical change, same as above, tacrine application group was the most significantly responded, following tDCS application group. Conclusion: From these results, confirm that tDCS application to rat with alzheimer's disease leads to positive effects on behavioral, cognitive function changes, and biochemical changes, lasting for certain period of time. This study, in particular, tDCS, which can change excitability of brain cells non-invasively, could provide basic data that is useful as a new treatment way for the patients with cognitive dysfunction.

• Archives of Pharmacal Research
• /
• v.28 no.3
• /
• pp.335-342
• /
• 2005

The effects of ginsenosides Rg$_3$(R) , Rg$_3$(S) and Rg$_5$/Rk$_1$ (a mixture of Rg$_5$ and Rk$_1$ 1:1, w/w), which are components isolated from processed Panax ginseng C.A. Meyer (Araliaceae), on memory dysfunction were examined in mice using a passive avoidance test. The ginsenosides Rg3(R), Rg3(S) or Rg$_5$/Rk$_1$, when orally administered for 4 days, significantly ameliorated the memory impairment induced by the single oral administration of ethanol. The memory impairment induced by the intraperitoneal injection of scopolamine was also significantly recovered by ginsenosides Rg3(S) and Rg$_5$/Rk$_1$. Among the three ginsenosides tested in this study, Rg$_5$/Rk$_1$ enhanced the memory function of mice most effectively in both the ethanol­and scopolamine-induced amnesia models. Moreover, the latency period of the Rg$_5$/Rk$_1$­treated mice was 1.2 times longer than that of the control (no amnesia) group in both models, implying that Rg$_5$/Rk$_1$ may also exert beneficial effects in the normal brain. We also evaluated the effects of these ginsenosides on the excitotoxic and oxidative stress-induced neuronal cell damage in primary cultured rat cortical cells. The excitotoxicity induced by glutamate or N­methyl-D-aspartate (NMDA) was dramatically inhibited by the three ginsenosides. Rg$_3$(S) and Rg$_5$/Rk$_1$ exhibited a more potent inhibition of excitotoxicity than did Rg$_3$(R). In contrast, these ginsenosides were all ineffective against the H$_2$O$_2$- or xanthine/xanthine oxidase-induced oxidative neuronal damage. Taken together, these results indicate that ginsenosides Rg$_3$(S) and Rg$_5$/Rk$_1$ significantly reversed the memory dysfunction induced by ethanol or scopolamine, and their neuroprotective actions against excitotoxicity may be attributed to their memory enhancing effects.

• Proceedings of the Ginseng society Conference
• /
• 2002.10a
• /
• pp.531-544
• /
• 2002

Ginseng is the best known and most popular herbal medicine used worldwide. Ameliorating effects of ginseng were observed on the models of scopolamine-induced, aged or hippocampal lesioned learning and memory deficits. Further beneficial effects of ginseng were observed on neuronal cell death associated with ischemia or glutamate toxicity. In spite of these beneficial effects of ginseng on the CNS, little scientific evidence shows at the cellular level. In the present study, we have employed cultures of rat hippocampal neurons and examined the direct modulation of ginseng on NMDA receptor-induced changes in $[Ca^{2+}]_i$ and -gated currents using fura-2-based digital imaging and perforated whole-cell patch-clamp techniques, respectively. We found that ginseng total saponins inhibited NMDA-induced but less effectively glutamate-induced increase in $[Ca^{2+}]_i$ Ginseng total saponins also modulated $Ca^{2+}$ transients evoked by depolarization with 50 mM KCI along with its own effects on $[Ca^{2+}]_i$. Among ginsenosides tested, ginsenoside $Rg_3$ was found to be the most potent component for ginseng actions on NMDA receptors. Furthermore, we examined the inhibitory effects ofbiotransformants of ginsenosides on NMDA receptor using purified stereoisomers of ginsenosides. 20(S)-ginsenoside $Rg_3$ and its metabolite, 20(S)-ginsenoside $Rh_3$, produced the strongest inhibition while 20(S)-ginsenoside $Rh_1$ and Compound K produced the moderate inhibition on NMDA-induced increase in $[Ca^{2+}]_i$. The data obtained suggest that the inhibition of NMDA receptors by ginseng, in particular by 20(S)-ginsenoside $Rg_3$ and its metabolite, 20(S)-ginsenoside $Rh_2$, could be one of mechanisms for ginsengmediated neuroprotective actions.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.45 no.1
• /
• pp.1-11
• /
• 2016

This study was conducted to investigate effect of the acetylcholinesterase inhibitor activity, the protective effect of the extract on SH-SY5Y cell death by $H_2O_2$, the memory improvement from scopolamine-induced rat. Moreover, the antioxidant activity of isorhamnetin from the dropwort (Oenanthe javanica) was investigated. Acetylcholinesterase inhibitor activity was highest (28.59%) in Hwasun O. javanica extract (H-OJE). H-OJE and Naju O. javanica extract (N-OJE) were not significantly different. SH-SY5Y cell death deceased to 37.23% and 36.68% for H-OJE and N-OJE, respectively, following treatment with the extracts. O. javanica extracts showed a protective effect against $H_2O_2$-induced neurotoxicity. Treatment with O. javanica extracts slightly improved scopolamine-induced (1 mg/kg, i.p.) memory impairment in rats. H-OJE contained the highest total phenolic and flavonoid contents of 117 mg/g and 30 mg gallic acid equivalents/g, respectively, and had a DPPH radical scavenging activity ($SC_{50}$) of $113.8{\mu}g/mL$ and ABTS radical scavenging activity of $48.2{\mu}g/mL$, which was higher than the other extracts. The thiobarbituric acid reactive substances value was highest (50.2%) in H-OJE. Antioxidant activity differed significantly among dropwort extracts. Isorhamnetin was known as one of the flavonoid and for having neuroprotective effect. So we analyzed acid-hydrolyzed O. javanica extract HPLC. The results were that peak at 14 min and spectrum of the extracts was consistent with standard solution. The results of LC/MS/MS analysis were that the extract and standard solution were confirmed total ion chromatogram at identical time, precursor ion was 317 $[M-H]^+$ m/z, product ion was 302 $[M-H]^+$ m/z. Overall, the results showed that the dropwort extract led to memory improvement and had antioxidant activity. Based on these finding, further research to investigate the production of ethanol extract of dropwort as a processed food is warranted.

• Nutrition Research and Practice
• /
• v.17 no.2
• /
• pp.192-205
• /
• 2023

BACKGROUND/OBJECTIVES: It is known that the renin-angiotensin system (RAS) in the brain could regulate cognitive functions as well as blood pressure. Inhibition of RAS for the improvement of cognitive function may be a new strategy, but studies so far have mostly reported on the effects of RAS inhibition by drugs, and there is no research on cognitive improvement through RAS inhibition of food ingredients. Therefore, this study investigated the effect of curcumin on blood pressure and cognitive function and its related mechanism in spontaneously hypertensive rat/Izm (SHR/Izm). MATERIALS/METHODS: Six-week-old SHR/Izm rats were divided into 5 groups: control group (CON), scopolamine group (SCO, drug for inducing cognitive deficits), positive control (SCO and tacrine [TAC]), curcumin 100 group (CUR100, SCO + Cur 100 mg/kg), and curcumin 200 group (CUR200, SCO + Cur 200 mg/kg). Changes in blood pressure, RAS, cholinergic system, and cognitive function were compared before and after cognitive impairment. RESULTS: The SCO group showed increased blood pressure and significantly reduced cognitive function based on the y-maze and passive avoidance test. Curcumin treatments significantly improved blood pressure and cognitive function compared with the SCO group. In both the CUR100 and CUR200 groups, the mRNA expressions of angiotensin-converting enzyme (ACE) and angiotensin II receptor type1 (AT1), as well as the concentrations of angiotensin II (Ang II) in brain tissue were significantly decreased. The mRNA expression of the muscarinic acetylcholine receptors (mAChRs) and acetylcholine (ACh) content was significantly increased, compared with the SCO group. CONCLUSIONS: The administration of curcumin improved blood pressure and cognitive function in SCO-induced hypertensive mice, indicating that the cholinergic system was improved by suppressing RAS and AT1 receptor expression and increasing the mAChR expression.