• Proceedings of the Plant Resources Society of Korea Conference
• /
• 2021.04a
• /
• pp.58-58
• /
• 2021

Although hypoxic/ischemic injury is thought to contribute to the incidence of Alzheimer disease (AD), the molecular mechanism that determines the relationship between hypoxia-induced β-amyloid (Aβ) generation and development of AD is not yet known. In this study, we investigated the protective effects of Acorus gramineus Soland. (AGS) on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced A β production in SH-SY5Y human neuroblastoma cells. Pretreatment of these cells with AGS significantly attenuated OGD/R-induced production of reactive oxygen species (ROS) and elevation of levels of malondialdehyde, nitrite (NO), prostaglandin E2 (PGE2), cytokines (TNF-α, IL-1β and IL-6) and glutathione, as well as superoxide dismutase activity. AGS also reduced OGD/R-induced expression of the apoptotic protein caspase-3, the apoptosis regulator Bcl-2, and the autophagy protein becn-1. Finally, AGS reduced OGD/R-induced Aβ production and cleavage of amyloid precursor protein, by inhibiting secretase activity and suppressing the autophagic pathway. Although supporting data from in vivo studies are required, our results indicate that AGS may prevent neuronal cell damage from OGD/R-induced toxicity.

• Korean Journal of Food Science and Technology
• /
• v.50 no.5
• /
• pp.517-527
• /
• 2018

The current study investigated in vitro anti-diabetic and neuroprotective effects of the ethyl acetate fraction in Actinidia arguta sprouts (EFAS), on $H_2O_2$ and high glucose-induced cytotoxicity in human neuroblastoma MC-IXC cells. EFAS had high total phenolic and total flavonoid contents. An assessment of 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging activity of EFAS, as well as its potential for inhibiting malondialdehyde production, indicated that EFAS may possess significant antioxidant properties. EFAS exerted inhibitory effects on ${\alpha}-glucosidase$ via glycemic regulation which forms advanced glycation end products. In addition, EFAS exhibited significant acetylcholinesterase inhibitory effects. Moreover, EFAS displayed protective effects against $H_2O_2$ and high glucose-induced cell death, and inhibited the generation of reactive oxygen species in MC-IXC cells. Finally, the main physiological compound of EFAS was identified via high performance liquid chromatography as a rutin.

• Journal of Life Science
• /
• v.29 no.2
• /
• pp.173-180
• /
• 2019

Amyloid ${\beta}$-protein ($A{\beta}$) is the principal component of senile plaques characteristic of Alzheimer's disease (AD) and elicits a toxic effect on neurons in vitro and in vivo. Many environmental factors, including antioxidants and proteoglycans, modify $A{\beta}$ toxicity. It is worthwhile to isolate novel natural compounds that could prove therapeutic for patients with AD without causing detrimental side effects. In this study, we investigated the in vitro neuroprotective effects of the ethyl acetate fraction of methanol extract of Ophiophogon japonicas (OJEA fraction). We used an MTT reduction assay to detect protective effects of the OJEA fraction on $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells. We also used a cell-based ${\beta}$-secretase assay system to investigate the inhibitory effect of the OJEA fraction on ${\beta}$-secretase activity. In addition, we performed an in vitro lipid peroxidation assay to evaluate the protective effect of the OJEA fraction against oxidative stress induced by $A{\beta}_{25-35}$ in PC12 cells. The OJEA fraction had strong protective effects against $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells and was strongly inhibitory to ${\beta}$-secretase activity, which resulted in the attenuation of $A{\beta}$ generation. In addition, the OJEA fraction significantly decreased malondialdehyde (MDA) content, which is induced by the exposure of PC12 cells to $A{\beta}_{25-35}$. Our results suggested that the OJEA fraction contained active compounds exhibiting a neuroprotective effect on $A{\beta}$ toxicity.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.45 no.7
• /
• pp.958-965
• /
• 2016

The objective of this study was to evaluate the antioxidant activity of green tea seed shell as an industrial byproduct. Green tea seed shell extract (GTSSE) was obtained by ethanol extraction, and the yield was $1.4{\pm}0.22%$. The radical scavenging activities [1,1-diphenyl-picrylhydrazyl and 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonic acid)], xanthine oxidase inhibition activity, and reducing power of GTSSE dose-dependently increased. To estimate the neuroprotective effect of GTSSE, viability was tested in HT22 mouse hippocampal cells. GTSSE treatment induced cytotoxicity at a concentration higher than $100{\mu}g/mL$ but not at a concentration lower than $50{\mu}g/mL$. Using this optimal concentration range, GTSSE treatment significantly increased cell viability in $H_2O_2$-treated HT22 cells. Further, GTSSE treatment increased superoxide dismutase activity and decreased the malonaldehyde level, a product of lipid peroxidation, in HT22 cells. Therefore, these results indicate that green tea seed shell extract may be useful for the development of antioxidant materials and have potential activity to prevent and treat neuro-degenerative diseases such as Alzheimer's disease.

• Neonatal Medicine
• /
• v.17 no.2
• /
• pp.181-192
• /
• 2010

Purpose: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. Methods: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% $CO_2$ incubators and the other groups were placed in 1% $O_2$ incubators (94% N2, 5% $CO_2$) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% $O_2$). Results: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. Conclusion: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.

• Korean Journal of Food Science and Technology
• /
• v.53 no.4
• /
• pp.423-433
• /
• 2021

This study was performed to examine the neuroprotective effect of the ethyl acetate fraction from Eucommia ulmoides oliver leaf (EFEL) on PM_2.5-induced cytotoxicity. EFEL had higher total phenolic and flavonoid contents than the other fractions. In ABTS and DPPH radical scavenging activities, the IC₅₀ of EFEL was measured as 212.80 and 359.13 ㎍/mL, respectively. To investigate the neuroprotective effect of EFEL, MTT and DCF-DA assays were performed on HT22, MC-IXC, and BV-2 cells. EFEL effectively decreased PM_2.5-induced intercellular reactive oxygen species (ROS) content and inhibited PM_2.5-induced cell death. In the results of protein expression related to cellular cytotoxicity on microglial cells (BV-2), EFEL had an improvement effect on cell apoptosis and inflammatory pathways. Rutin and chlorogenic acid were identified as the main physiological compounds. Moreover, it was expected that EFEL, including rutin and chlorogenic acid, could be functional food substances with neuroprotective effects against PM_2.5-induced oxidative stress.

• The Journal of Korean Obstetrics and Gynecology
• /
• v.22 no.1
• /
• pp.15-30
• /
• 2009

Purpose: In this rapidly aging society, the research and development of traditional oriental medicine treatment is one of the critical factors to protect the increasing neuro-degenerative disorders. In this study, we wanted to verify the effect of Yukul-tang (YUT) on neuro-degenerative disease model by assessing the antioxidant and anti-inflammation effects. Methods: To assess the antioxidant effects of YUT, we carried out DPPH radical and ABTS radical scavenging assays and determined the total polyphenolic contents in YUT. To evaluate the neuro-protective effects of YUT, we performed the MTT and ROS assays and TH immunohistochemistry, NO and TNF-${\alpha}$ assays in SH-SY5Y or mesencephalic dopaminergic neurons damaged by 6-OHDA. Results: The treatment of YUT showed eliminating effects on DPPH radical and ABTS radical. it showed deterring effects on ROS, NO and TNF-${\alpha}$ and protecting effects on TH-positive cell in SH-SY5Y cells or mesencephalic dopaminergic neurons. Especially in the case of the treatment of YUT with 0.2ug/mL + 6-OHDA 10uM, the protective effect on dopaminergic neurons was most outstanding. Conclusion: In this study, we have demonstrated that YUT has an antioxidant effect and a neuro-protective effect on neuro-degenerative disease model caused by neurotoxin such as 6-OHDA. The results of our present study suggest that YUT can be useful agent to prevent and to treat neuro-degenerative diseases.

• Journal of Life Science
• /
• v.32 no.7
• /
• pp.550-566
• /
• 2022

Stroke is among the leading causes of death and long-term physical and cognitive disabilities worldwide, affecting an estimated 15 million people annually. The pathophysiological process of stroke is complicated by multiple and coordinated events. The breakdown of the blood-brain barrier (BBB) in people with stroke can significantly contribute to the development of ischemic brain injury. Therefore, BBB disruption is recognized as a hallmark of stroke; thus, it is important to develop novel therapeutic strategies that can protect against BBB dysfunction in ischemic stroke. Traditional medicines are composed of natural products, which represent a promising source of new ingredients for the development of conventional medicines. Indeed, several studies have shown the effectiveness of Korean medicine on stroke, highlighting the value of Korean medicinal treatment for ischemic stroke. This review summarizes the current information and underlying mechanisms regarding the ameliorating effects of the formula, decoction, herbs, and active components of traditional Korean medicine on cerebral ischemia-induced BBB disruption. These traditional medicines were shown to have protective effects on the BBB in many cellular and animal ischemia models of stroke, and experiments in various animal species, such as mice and rats. In addition, they showed brain-protective effects by protecting the BBB through the regulation of tight junction proteins and matrix metalloproteinase-9, reducing edema, neuroinflammation, and neuronal cell death. We hope that this review will help promote further investigation into the neuroprotective effects of traditional Korean medicines and stimulate the performance of clinical trials on Korean herbal medicine-derived drugs in patients with stroke.

• KOREAN JOURNAL OF CROP SCIENCE
• /
• v.67 no.4
• /
• pp.305-318
• /
• 2022

To minimize the effects of aging-related comorbidities and to maintain a good quality of life and physical independence for a longer period, the improvement of lifestyle and dietary habits is essential, and healthy foods can be helpful. Among them, medicinal plant such as ginseng (Panax ginseng) and bellflower (Platycodon grandiflorum) contain natural functional substances and have been used for disease treatment and prevention since ancient times. This review summarizes the scientific of these treatments basis by investigating the pharmacological and pharmacokinetic effects of major functional substances on the aging-related health effects of Panax ginseng and Platycodon grandiflorum. The main functional substances of Panax ginseng and Platycodon grandiflorum are saponins, which have a similar molecular structure and confirmed anti-inflammatory, antioxidant, neuroprotective, anticancer, and anti-metabolic syndrome effects (improvement of hypertension, dyslipidemia, diabetes, and obesity). Both types of saponins in Panax ginseng (Ginseonside) and Platycodon grandiflorum (Platycoside) have very low absorption profiles in their purified state, but methods to increase absorption in the body through extraction or fermentation have been studied.

• Journal of Ginseng Research
• /
• v.47 no.2
• /
• pp.302-310
• /
• 2023

Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this damage could cause neurodegeneration. We previously reported that non-saponin fraction with rich polysaccharide (NFP) from Korean Red Ginseng (KRG) showed neuroprotective effects in AD. However, precise molecular mechanism of the therapeutic effects of NFP from KRG in AD still remains elusive. Methods: To investigate the therapeutic mechanisms of NFP from KRG on AD, we conducted proteomic analysis for frontal cortex from vehicle-treated wild-type, vehicle-treated 5XFAD mice, and NFP-treated 5XFAD mice by using nano-LC-ESI-MS/MS. Metabolic network analysis was additionally performed as the effects of NFP appeared to be associated with metabolism according to the proteome analysis. Results: Starting from 5,470 proteins, 2,636 proteins were selected for hierarchical clustering analysis, and finally 111 proteins were further selected for protein-protein interaction network analysis. A series of these analyses revealed that proteins associated with synapse and mitochondria might be linked to the therapeutic mechanism of NFP. Subsequent metabolic network analysis via genome-scale metabolic models that represent the three mouse groups showed that there were significant changes in metabolic fluxes of mitochondrial carnitine shuttle pathway and mitochondrial beta-oxidation of polyunsaturated fatty acids. Conclusion: Our results suggested that the therapeutic effects of NFP on AD were associated with synaptic- and mitochondrial-related pathways, and they provided targets for further rigorous studies on precise understanding of the molecular mechanism of NFP.