• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.47-56
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• 1998

In the present study, we assayed a number of compounds isolated from Panax ginseng C. A. Meyer (Araliaceae) for an ability to protect rat cortical cell cultures from the deleterious effects of the neurotoxicant, glutamate. We found that ginsenosides Rbl and Rg3 significantly attenuated glutamate-induced neurotoxicity. Brief exposure of cultures to excess glutamate caused extensive neuronal death. Glutamate-induced neuronal cell damage was significantly reduced by pretreatment with Rbl and Rgl. Ginsenosides Rbl and Rg3 inhibited the overproduction of nitric oxide which routinely follows glutamate neurotoxicity and preserved the level of superoxide dismutase in glutamate-treated cells. Furthermore, in cultures treated with glutamate, these ginsenosides inhibited the formation of malondialdehyde, a compound produced during lipid peroxidation, and diminished the influx of calcium. These results show that ginsenosides Rbl and Rg1 exerted significant neuroprotective effects on cultured cortical cells. As such, these compounds may be efficacious in protecting neurons from oxidative damage produced by exposure to excess glutamate.

• Archives of Pharmacal Research
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• v.26 no.10
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• pp.800-804
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• 2003

The effects of KR-31378, a neuroprotective agent for ischemia-reperfusion damage, on liver microsomal cytochrome P450s (CYPs) were investigated in male Sprague Dawley rats. When rats were treated orally with KR-31378 for 7 consecutive days, CYP3A-selective erythromycin N-demethylase (ERDM) activity was significantly induced in a dose-dependent manner. In Western immunoblotting, CYP 3A proteins were clearly induced by treatment with KR-31378. Within 24 h after treatment with 80 mg/kg of KR-31378, ERDM activity was induced in liver microsomes in accompanied by induction of the level of CYP 3A proteins. The present results suggest that KR-31378 might modulate the expression of CYP 3A enzymes in humans.

• The Korea Journal of Herbology
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• v.25 no.2
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• pp.71-79
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• 2010

Objectives : In this study, the neuroprotective effects of modified Boyanghwano-Tang (mBHT) and the major medicinal plants, Astragali Radix(AR) and Salviae Miltiorrhizae Radix(SMR) were investigated in transient middle cerebral artery occlusion (tMCAO)-induced ischemic stroke of rats. Methods : mBHT(400 mg/kg) and AR(154 mg/kg) or SMR(62 mg/kg) water extract orally injected in rats after 90 min occlusion of MCA and then allow reperfusion to 24 h. Brain infarction was measured by TTC staining and the expressions of NOS isoforms and apoptotic molecules were determined in ischemic brain by Western blot. Results : The results showed that mBHT has stronger neuropreotective property through inhibitions of the PARP cleaved and caspase-3 activation in ischemic rats, and could reduced infarction volumes comparison of those of AR or SMR, respectively. While, AR extract has an angiogenic property through increasing the expressions of eNOS and VEGF, and SMR extract has a strong anti-inflammatory effects through inhibition of iNOS expression in ischemic brains. Conclusions : These results suggest that mBHT has multifactorial therapeutic advantages through anti-apoptosis, anti-inflammation and angiogenesis for ischemic stroke based on a synergistic combination of ingradients rather than monotherapy.

• Journal of Korean Neurosurgical Society
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• v.60 no.4
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• pp.391-396
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• 2017

Objective : To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. Methods : Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. Results : GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. Conclusion : Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.

• Journal of Ginseng Research
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• v.45 no.2
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• pp.211-217
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• 2021

The treatments of nervous system diseases (NSDs) have long been difficult issues for researchers because of their complexity of pathogenesis. With the advent of aging society, searching for effective treatments of NSDs has become a hot topic. Ginseng polysaccharides (GP), as the main biologically active substance in ginseng, has various biological properties in immune-regulation, anti-oxidant, anti-inflammation and etc. Considering the association between the effects of GP and the pathogenesis of neurological disorders, many related experiments have been conducted in recent years. In this paper, we reviewed previous studies about the effects and mechanisms of GP on diseases related to nervous system. We found GP play an ameliorative role on NSDs through the regulation of immune system, inflammatory response, oxidative damage and signaling pathway. Structure-activity relationship was also discussed and summarized. In addition, we provided new insights into GP as promising neuroprotective agent for its further development and utilization.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.408-415
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• 2023

Alzheimer's disease constitutes a large proportion of all neurodegenerative diseases and is mainly caused by excess aggregation of amyloid beta (Aβ), which results in oxidative stress, inflammation, and apoptosis in the neurons. Populus tomentiglandulosa belongs to the Salicaceae family and is widely distributed in Korea; the antioxidant activities of the extract and fractions from P. tomentiglandulosa have been demonstrated in previous studies. Specifically, the ethyl acetate (EtOAc) fraction of P. tomentiglandulosa (EtOAc-PT) shows the most powerful antioxidative activity. Therefore, the present study investigates the protective effects of EtOAc-PT against neuronal damage in Aβ_25-35-stimulated SH-SY5Y cells. EtOAc-PT restored cell viability significantly as well as inhibited the levels of reactive oxygen species and lactate dehydrogenase release compared to the Aβ_25-35-induced control group. Furthermore, the inflammation- and apoptosis-related protein expressions were investigated to demonstrate its neuroprotective mechanism. EtOAc-PT downmodulated the expressions of inducible nitric oxide synthase, cyclooxygenase-2, B-cell lymphoma 2 associated X, and B-cell lymphoma 2. Thus, the findings show that EtOAc-PT has protective effects against Aβ_25-35 by suppressing oxidative stress, inflammation, and apoptosis.

• Journal of Oriental Neuropsychiatry
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• v.22 no.2
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• pp.85-105
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• 2011

Objectives : The purpose of this study was to characterize the neuroprotective effects and anxiolytic-like effects of Gongjin-dan and Polygala japonica, Polygala tenuifolia, Acorus gramineus mixed pills(G.J.D-P.P.A.). Methods : The neuroprotective effects of G.J.D-P.P.A. determined by the passive avoidance and Y-maze tasks and Morris water maze task, and the anxiolytic-like effects of the G.J.D-P.P.A. using an elevated plus-maze(EPM) in mice. Results : Drug-induced amnesia was induced by treating animals with scopolamine(1 mg/kg, i.p.). A single G.J.D-P.P.A.(400 and 800 mg/kg) administration significantly enhanced cognitive function and attenuated scopolamine-induced cognitive impairments as determined by the passive avoidance and Y-maze tasks(P < 0.05) and also reduced escape-latency on the Morris water maze task(P < 0.05). The administration of GJD-PPA(400 and 800 mg/kg) significantly increased the percentage of time spent in open arms and entries into the open arms of the EPM compared with saline-treated control group(P < 0.05). Moreover, there were no changes in the locomotor activity and myorelaxant effects in any group compared with saline-treated control group. Conclusions : These results suggest that GJD-PPA dramatically possesses the anti-amnestic and cognitive-enhancing activities related to the memory processes, and promotes the anxiolytic-like activity in mice.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.303.2-304
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• 2002

Wogonin. a flavonoid originated from the root of Scutellaria baicalensis Georgi. is known to exhibit potent anti-inflammatory effects and variable degrees of antioxidant and free radical scavenging effects depending on the experimental systems. In addition. wogonin has been reported to protect neurons from excitotoxic and oxidative injuries in primary cultured rat cortical cells. (omitted)

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.11
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• pp.1580-1588
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• 2016

The 70% ethanol extract from Adenophora triphylla showed a strong antioxidant effect and reduced cytotoxicity of $H_2O_2$ in SK-N-SH cells. The chloroform fraction from A. triphylla extract (AT-CH) among the six fractions showed strong DPPH radical and intracellular reactive oxygen species (ROS) scavenger effects and the highest protective effect against $H_2O_2$-induced SK-N-SH cell death. Bioactivity compounds were purified from AT-CH, and the chemical structures of the compounds were determined as ${\beta}$-sitosterol and daucosterol on the basis of $^1H-NMR$, $^{13}C-NMR$, and EI mass spectra. ${\beta}$-Sitosterol and daucosterol also had protective effects against oxidative stress in SK-N-SH cells. Phospho-p38 MAPK levels were elevated by $H_2O_2$ but were inhibited by treatment with AT-CH and phytosterols (${\beta}$-sitosterol and daucosterol) isolated from AT-CH. These results suggest that AT-CH has brain neuroprotective effects against oxidative stress ($H_2O_2$) by inhibiting activation of p38 pathways and scavenging intracellular ROS.

• Clinical and Experimental Pediatrics
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• v.52 no.1
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• pp.105-110
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• 2009

Purpose : Perinatal asphyxia is an important cause of neonatal mortality and subsequent lifelong neurodevelopmental handicaps. Although many treatment strategies have been tested, there is currently no clinically effective treatment to prevent or reduce the harmful effects of hypoxia and ischemia in humans. Erythropoietin (Epo) has been shown to exert neuroprotective effects in various brain injury models although the exact mechanisms through which Epo functions are not completely understood. This study investigates the effect of Epo on hypoxic-ischemic (HI) brain injury and the possibility that its neuroprotective actions may be associated with iron-mediated metabolism. Methods : HI brain injury was produced in 7-day-old rats by unilateral carotid artery ligation followed by hypoxia with 8% oxygen for 2 h. At the end of HI brain injury, the rats received an intraperitoneal injection of 5,000 units/kg erythropoietin. Random premedication with iron, deferoxamine, iron-deferoxamine, or saline were performed 23 d before HI brain injury. The severity of the brain injury was assessed at 7 d after HI. Results : Single Epo treatment post-HI brain injury reduced the gross and histopathological findings of brain injury. Iron premedication did not increase the incidence or severity of the injury as measured by the damage score. Deferoxamine administration before HI brain injury improved the brain injury as compared to no treatment or Epo treatment. Conclusion : These findings indicate that Epo provides neuroprotective benefits after HI in the developing brain. These findings suggest that Epos neuroprotective actions may involve reducing iron in tissues that mediate the formation of free radicals.