• Journal of Life Science
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• v.26 no.12
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• pp.1458-1465
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• 2016

We investigated the neuroprotective effect of an ethanol extract from Asparagus cochinchinensis (AC) against glutamate-induced toxicity in the HT22 hippocampal cell, which is an ideal in vitro model for oxidative stress. The neuroprotective effects of AC in HT22 cells were evaluated by analyzing cell viability, lactate dehydrogenase (LDH), flow cytometry for cell death types, reactive oxygen species (ROS), mitochondria membrane potential (MMP), and Western blot assays. In the cell death analysis, AC treatment resulted in significantly attenuated glutamate-induced loss of cell viability with a decrease in LDH release. AC treatment also reduced glutamate-induced apoptotic cell death. In the ROS and MMP analysis, AC treatment inhibited the elevation of intracellular ROS induced by glutamate exposure and the disruption of MMP. In oxidative stress-related proteins analysis, AC treatment inhibited the expression of poly ADP ribose polymerase and heme oxygenase-1 by glutamate. These results indicate that AC exerts a significant neuroprotective effect against glutamate-induced hippocampal damage by decreasing ROS production and stabilizing MMP. Thus, AC potentially provides a new strategy for the treatment of oxidative stress-related diseases.

• The Journal of the Convergence on Culture Technology
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• v.8 no.3
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• pp.291-296
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• 2022

This study was conducted on curcumin which had increased bioavailability as a potential AChE inhibitor for the treatment of neurodegenerative diseases. The purpose of this study is to confirm the in vitro neuroprotective effect on Aricumin (turmeric extract). To confirm the neuroprotective effect, AChE inhibition for Aricumin was evaluated, and cell viability was analyzed for HT-22cell, and oxidative stress (glutamate, H₂O₂)-induced HT-22 cytotoxicity was evaluated. As a result of the change in the AChE inhibition rate of Aricumin (Turmeric extract), it was confirmed that Aricumin at a concentration of 39.06㎍/ml or higher inhibited AChE activity by about 20% and more. And it was confirmed that the cytotoxicity of HT-22 cells induced by oxidative stress (Gluamate 5 mM and H₂O₂ 500 µM) was significantly inhibited from 0.01 to 0.1 mg/ml concentration (p<005). These results suggest that Aricumin (turmeric extract) have potential neuroprotective effects.

• Journal of Life Science
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• v.34 no.1
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• pp.37-47
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• 2024

FUN14 domain-containing protein 1 (FUNDC1), an outer mitochondrial membrane protein, contributes to removal of damaged mitochondria through mitophagy. In this study, to elucidate the role of the FUNDC1 in the amyloid beta peptide (A_β)-induced neuropathy, changes in the degree of mitochondrial dysfunction and cell injury caused by A_β treatment were examined in the HT-22 neuronal cells in which the FUNDC1 expression was transiently silenced or overexpressed. We found that A_β treatment causes a time-dependent decrease of the FUNDC1 expression. In the A_β-treated cells, there were a drop in MTT reduction ability, depletion of cellular ATP, disruption of mitochondrial membrane potential, stimulation of cellular ROS production, and increased mitochondrial Ca²⁺ load. Activation of caspase-3 and induction of apoptotic cell death were also observed. Transient silencing of the FUNDC1 expression by transfection with the FUNDC1 small interfering RNA per se caused mitochondrial dysfunction and apoptotic cell death like the effect of A_β treatment. Conversely, in cells in which the FUNDC1 was transiently overexpressed by FUNDC1-Myc transfection, overexpression itself had no effect on the mitochondrial functional integrity and cell survival but showed a significant prevention effect against mitochondrial and cell injury caused by A_β treatment. Overall, these results suggest that the FUNDC1 is importantly involved in the A_β-induced mitochondrial dysfunction and cell injury in the HT-22 neuronal cells.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.250-257
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• 2023

Glutamate is an excitatory neurotransmitter distributed in the central nervous system of mammals. However, high concentrations of glutamate are known to cause neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and stroke by causing nerve cell death. In this study, the antioxidant activity and neuroprotective effect of subtropical natural products were analyzed. Among 11 subtropical plant extracts mainly tested, Sallacca wallichiana extract (SE) showed the greatest free radical scavenging activity. Then, we confirmed through WST-1 assay that SE protected HT22 cells against glutamate-induced cell death in a concentration-dependent manner. The protective effects of SE against glutamate-induced apoptosis in HT22 cells were also confirmed by flow cytometry analysis using Annexin V/PI double staining. We also confirmed using H₂DCF-DA single staining that SE inhibits glutamate-induced intracellular reactive oxygen species. And we were confirmed through that SE inhibited glutamate-induced phosphorylation of Mitogen-activated Protein kinases. Consequently, our results propose that SE may contribute to the development of therapeutics to prevent neurodegenerative diseases.

• Journal of Life Science
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• v.22 no.1
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• pp.55-61
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• 2012

Akt is known to play an important role in cell proliferation and differentiation, and is also over-expressed in several types of cancer cells. In this study, we explored the anti-proliferative effects of selenium in HT-29 colon cancer cells, mediated through effects on Akt and COX-2. Selenium treatments at different concentrations and for different durations inhibited proliferation of HT-29 colon cancer cells and increased apoptotic cell death. Selenium treatment decreased Akt phosphorylation and COX-2 expression. Treatment with LY294002 (an Akt inhibitor) decreased proliferation of HT-29 cells, while a combined treatment with LY294002 and selenium resulted in even further decreases in cell proliferation. Inactivation of Akt by Akt siRNA treatment abolished these inhibitory effects on cell growth. COX-2 expression decreased in Akt transfected cells compared to non-transfected cells. These results suggest that selenium induced both anti-proliferative and apoptotic effects by inhibiting Akt phosphorylation and COX-2 expression. Selenium treatment also appeared to induce synergistic anti-proliferative effects by inhibition of Akt in HT-29 colon cancer cells.

• The Korea Journal of Herbology
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• v.22 no.2
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• pp.65-72
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• 2007

Objectives : In this study, we investigate that Euphorbiae lathyridis Semen extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Euphorbiae lathyridis Semen was extracted from the Semen of the plant using 80% Methanol. The Euphorbiae lathyridis Semen extract was treated to different concentrations for 24 hr, 4Shr or 72hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Westem blot. Results : Exposure to Euphorbiae lathyridis Semen extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Euphorbiae lathyridis Semen extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Euphorbiae lathyridis Semen extract induces DNA fragmentation in HT-29 cells. Furthermore, Euphorbiae lathyridis Semen extract induces cell apoptosis through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion : Euphorbiae lathyridis Semen extract induces apoptosis in human colon cancer cells, therefore, we suggest that Euphorbiae lathyridis Semen extract can be used as a novel class of anti-cancer drugs.

• Journal of Korean Clinical Nursing Research
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• v.21 no.2
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• pp.234-242
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• 2015

Purpose: The purpose of this study was to investigate the levels of knowledge and medication adherence to hormonal therapy (HT) and to identify the factors influencing medication adherence for patients with breast cancer. Methods: Data were collected from 136 patients undergoing adjuvant HT for breast cancer in 3 general hospitals from July 1 to August 14 in 2014 using self-report questionnaires. Data were analyzed using descriptive statistics, independent t-test, ANOVA, $Scheff{\grave{e}}$ test, and multiple regression. Results: The average of knowledge about HT was $5.15{\pm}2.22$ (Max 9), and that of medication adherence was $5.76{\pm}1.65$ (Max 8). Younger age, shorter duration of HT, more active participation in decision making for treatment, positive perception for impacts of HT, and stronger belief in cure were influencing factors on higher adherence level. Age, duration of HT, and perception on the impacts of hormonal therapy, and belief in cure explained 25.2% of the adherence. Conclusion: To improve the treatment adherence to hormonal therapy, patient education and involvement in decision making, and the tailored intervention for the patients with older age, and long treatment period of HT are needed. Additionally, the strategies for diminishing unintentional forgetting is necessary to be developed.

• Clinical and Experimental Pediatrics
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• v.52 no.9
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• pp.984-990
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• 2009

Purpose : Being small for gestational age (SGA) is a risk factor of short stature in children. Genetic background such as mid-parental height (MPH) is known to influence growth of children born SGA. We studied the relationship between growth of children born SGA and MPH and studied the effects of insulin-like growth factor (IGF-I) and insulin-like growth factor binding protein 3 (IGFBP-3) on postnatal growth in children born SGA according to MPH. Methods : Forty-nine neonates born SGA were included in this study. We defined corrected height standard deviation score (cHtSDS) by modified height SDS (HtSDS) based on their MPH. We categorized subjects into group 1 consisting of children with cHtSDS ${\geq}0$ (n=35) and group 2 consisting of children with cHtSDS <0 (n=14), and compared IGF-I and IGFBP-3 between the two groups. Results : The HtSDSs and cHtSDSs in groups 1 and 2 were $0.06{\pm}1.05$ vs. $-0.95{\pm}0.85$ (P=0.000) and $0.78{\pm}0.93$ vs. $-0.46{\pm}0.67$ (P=0.000), respectively. IGF-I SDS was higher in group 1 than in group 2 ($2.82{\pm}3.69$ vs. $0.23{\pm}2.42$, P=0.012). Total cHtSDS ($0.42{\pm}1.03$) was significantly higher than HtSDS ($-0.22{\pm}1.10$) (P=0.000). Conclusion : Our results show that cHtSDS differs significantly from HtSDS. Growth assessment by standardized growth curve does not uniformly show effects of genetic factors. A more accurate assessment of growth uses a personalized corrected growth curve that considers the genetic factor measured by MPH.

• The Korea Journal of Herbology
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• v.22 no.4
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• pp.51-58
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• 2007

Objectives : Investigation of the memory and cognitive enhancing effect of HT008-1 in scopolamine induced amnesia mice. Methods : At 60 min before acquisition trials, HT008-1 (30, 100, 300 mg/kg p.o.) was administered, and 30 min later, mice were injected with scopolamin (1.0 mg/kg, i.p.). In the passive avoidance test, acquisition trials were carried out 30 min after a single scopolamine treatment. Retention trials were carried out 24h after acquisition trials. Y-maze test was carried out 30 min after a single scopolamine treatment. Spontaneous alternation behavior during an 8-min session was recorded. Inhibitory effects of HT008-1 (0.01, 0.1, 1.0 mg/ml) on AChE activity was measured. Result : HT008-1 ameliorated scopolamine-induced learning impairments and spatial cognitive function in passive avoidance and Y-maze test, respectively. Moreover HT008-1 showed a significant inhibitory effect on AChE activity. Discussion: This study presented that eMultiherb mixture HT008-1 enhanced learning memory and spatial cognitive function in scopolamine-induced amnesia mice. These results suggest that the effect of HT008-1 may be dependent on the inhibition of AChE activity.

• The Journal of Korean Medicine
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• v.39 no.1
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• pp.35-43
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• 2018

Objectives: In the brain, glutamate is the most important excitable neurotransmitter in physiological and pathological conditions. However, the high level of glutamate induces neuronal cell death due to exitotoxicity and oxidative stress. The present study investigated to evaluate a possible neuroprotective effect of furosin isolated from Euphorbia helioscopia against glutamate-induced HT22 cell death. Methods: Furosin was isolated from methanol extract of Euphorbia helioscopia and examined whether it protects glutamate-induced neuronal cell death. The cell viability was determined using Ez-Cytox assay. Anti-oxidative effect of furosin was determined by DPPH scavenging activities, and the levels of intracellular reactive oxygen species (ROS) were determined by the fluorescent intensity after staining the cells with $H_2DCFDA$. To evaluate apoptotic cell death, we performed nuclear staining and image-based cytometeric analysis. Results: The cell viability was significantly increased by treatement with furosin compared with the treatment with glutamate. Furosin showed a strong DPPH radical scavenging activity ($EC50=1.83{\mu}M$) and prevented the accumulation of intra cellular ROS. Finally, the presence of 50 and $100{\mu}M$ furosin significantly the percentage of apoptotic cells compared with glutamate treatment. Conclusion: The present study found that furosin is a potent neuroprotectant against glutamate-induced oxidative stress through inhibition of apoptotic cell death induced by glutamate. Therefore, the present study suggests that furosin as a bioactive compound of E. helioscopia can be a useful source to develop a drug for the treatment of neurodegenerative diseases and acute brain injuries.