• Food Science and Preservation
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• v.31 no.1
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• pp.99-111
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• 2024

The antioxidant potentials of ethanolic extracts derived from Aster yomena (A. yomena) were evaluated by assessing their total phenolic and flavonoid contents and radical scavenging activities. Our findings revealed that the 60% ethanolic extract of A. yomena exhibited the most robust antioxidant properties among all extracts tested. Specifically, the IC₅₀ values for the 2,2'-azino-bis (3-ethyl benzothiazoline-6-sulfonic acid) and 1,1-diphenyl-2-picrylhydrazyl radical scavenging activities of the 60% ethanolic extract from A. yomena were determined to be 1,640.30 ㎍/mL and 2,655.10 ㎍/mL, respectively. Moreover, the inhibitory effect on malondialdehyde increased with the 60% ethanolic extract from A. yomena. To assess the neuroprotective effects, we examined the impact of the 60% ethanolic extract from A. yomena against H₂O₂-induced cytotoxicity in HT-22 (mouse hippocampal neuronal cell line) and SK-N-MC (human neuroblastoma cell line) cells. The results demonstrated a significant improvement in cell viability and reduced intracellular oxidative stress. Furthermore, the major bioactive compounds present in the 60% ethanolic extract from A. yomena were identified as chlorogenic acid and rutin through high-performance liquid chromatography (HPLC) analysis.

• Clinical and Experimental Pediatrics
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• v.46 no.7
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• pp.702-709
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• 2003

Purpose : $IFN{\gamma}$ sentitizes many tumor cells to $TNF{\alpha}$ and FASL-mediated apoptosis by enhancing the expression of TNF or FAS/CD95 receptor and modulating the activation of caspase and Bcl-2 family. It has been reported that $IFN{\gamma}$ and $TNF{\alpha}$ synergistically caused differentiation and growth inhibition of neuroblastoma cells. Even though some neuroblastoma cell express FASR/FASL on the cell surface, they could not induce apoptosis by ligation of the FAS/CD95 receptor. But the treatment of $IFN{\gamma}$ is reported to induce apoptosis in some neuroblastoma cell lines through the CD95/CD95L autocrine circuit. In this study, we examined whether $IFN{\gamma}$ could affect $TNF{\alpha}$ and agonistic FAS/CD95 antibody(CH-11)-induced apoptosis against neuroblastoma cell lines that had shown diverse drug sensitivity and resistance. Methods : CHLA-15, CHLA-90 and LA-N-2 neuroblastoma cells were cultured in IMDM and treated with recombinant $IFN{\gamma}$, $TNF{\alpha}$ and CH-11 antibody. Cell viability was measured by DIMSCAN with a fluorescent calcein-AM. Apoptosis was analyzed through flow cytometry using Annexin V-PE and 7-ADD staining and confirmed by pancaspase and caspase-8 blocking experiments. The expression of TNF RI and FAS/CD95 receptor was evaluated by flow cytometry using the corresponding antibody and PE-conjugated secondary antibody. Results : $IFN{\gamma}$ or $TNF{\alpha}$ alone had no demonstrable cytotoxic effects, whereas both cytokines in combination induced apoptosis synergistically in CHLA-15 and CHLA-90 cells. Although there was no cytotoxicity with the ligation of CH-11 alone in CHLA-90 cells, pretreatment of $IFN{\gamma}$ increased the sensitivity of CH-11-mediated apoptosis. The expression of TNFRI and FAS/CD95R were non-specifically enhanced after treatment of $IFN{\gamma}$ without relation to sensitivity to $TNF{\alpha}$ and CH-11. This finding suggest up-regulation of both receptors may contribute to sensitization of $TNF{\alpha}$ and CH-11-mediated apoptosis by $IFN{\gamma}$ in only sensitive cell lines. Conclusion : $IFN{\gamma}$ induced sensitization of $TNF{\alpha}$ and agonistic FAS/CD95 antibody-mediated apoptosis on some neuroblastoma cells through up-regulation of TNFRI and FAS/CD95 receptor.

• Molecules and Cells
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• v.20 no.2
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• pp.280-287
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• 2005

The insulin-mediated Ras/mitogen-activated protein (MAP) kinase cascade was examined in SK-N-BE(2) and PC12 cells, which can and cannot produce reactive oxygen species (ROS), respectively. Tyrosine phosphorylation of the insulin receptor and insulin receptor substrate 1 (IRS-1) was much lower in SK-N-BE(2) cells than in PC12 cells when the cells were treated with insulin. The insulin-mediated interaction of IRS-1 with Grb2 was observed in PC12 but not in SK-N-BE(2) cells. Moreover, the activity of extracellular-signal-related kinase (ERK) was much lower in SK-N-BE(2) than in PC12 cells when the cells were treated with insulin. Application of exogenous $H_2O_2$ caused increased tyrosine phosphorylation and Grb2 binding to IRS-1 in SK-N-BE(2) cells, while exposure to an $H_2O_2$ scavenger (N-acetylcysteine) or to a phophatidylinositol-3 kinase inhibitor (wortmannin), and expression of a dominant negative Rac1, decreased the activation of ERK in insulin-stimulated PC12 cells. These results indicate that the transient increase of ROS is needed to activate ERK in insulin-mediated signaling and that an inability to generate ROS is the reason for the insulin insensitivity of SK-N-BE(2) cells.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.5
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• pp.163-169
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• 2007

The neurotoxicity of amyloid $\beta(A\beta)$ is associated with an increased production of reactive oxygen species and apoptosis, and it has been implicated in the development of Alzheimer's disease. While(-)-epigallocatechin-3-gallate(EGCG) suppresses $A\beta$-induced apoptosis, the mechanisms underlying this process have yet to be completely clarified. This study was designed to investigate whether EGCG plays a neuroprotective role by activating cell survival system such as protein kinase C(PKC), extracellular-signal-related kinase(ERK), c-Jun N-terminal kinase(JNK), and anti-apoptotic and pro-apoptotic genes in SH-SY5Y human neuroblastoma cells. One ${\mu}M\;A{\beta}_{1-42}$ decreased cell viability, which was correlated with increased DNA fragmentation evidenced by DAPI staining. Pre-treatment of SH-SY5Y neuroblastoma cells with EGCG($1{\mu}M$) significantly attenuated $A{\beta}_{1-42}$-induced cytotoxicity. Potential cell signaling candidates involved in this neuroprotective effects were further examined. EGCG restored the reduced PKC, ERK, and JNK activities caused by $A{\beta}_{1-42}$ toxicity. In addition, gene expression analysis revealed that EGCG prevented both the $A{\beta}_{1-42}$-induced expression of a pro-apoptotic gene mRNA, Bad and Bax, and the decrease of an anti-apoptotic gene mRNA, Bcl-2 and Bcl-xl. These results suggest that the neuroprotective mechanism of EGCG against $A{\beta}_{1-42}$-induced apoptotic cell death includes stimulation of PKC, ERK, and JNK, and modulation of cell survival and death genes.

• Journal of Life Science
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• v.23 no.8
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• pp.1019-1024
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• 2013

The aims of this study were to determine antioxidation effect and neuroblastoma cell protection effect of donkey's bone and skin extracts (DBSE). DBSE was extracted by a pressure-cooker for 48 h and lyophilized. The 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity was significantly increased with increased doses of DBSE and 40 mg/ml of DBSE showed 95.43% of the DPPH scavenging effect, which was equivalent to 1 mg/ml of vitamin C. The 2,2'-azino-bis (3-ethylbenzothiazoline-6- sulphonic acid) (ABTS) radical scavenging activity was also increased in a dose-dependent manner, and 20 mg/ml of DBSE showed 88.73% of the ABTS scavenging effect. The oxygen radical absorbance capacity (${\mu}M$ Trolox equivalent) of DBSE was significantly increased at a concentration of 10 mg/ml, which showed $132.53{\mu}M$ TE. The viability of oxidatively stressed brain cells induced by $500{\mu}M\;H_2O_2$ was protected by DBSE at concentrations greater than $50{\mu}M$. Cell viability after DBSE treatment at 50 and $100{\mu}g/ml$ was 53.78 and $54.34{\mu}M$ TE, respectively. There was no significant difference between both doses; however, 200 and $500{\mu}g/ml$ of DBSE showed 59.74 and 66.08% of cell viability, respectively indicating that DBSE protected SK-N-SH from oxidation stress. These results suggest that DBSE may have potential to be used as natural antioxidants in food industry, while in vivo evidence is necessary to support DBSE's in vitro-based antioxidative efficiency.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.244-252
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• 1998

Ginsenoside Rh, (G-Rh,) from Panax ginseng induced morphological features of apoptosis and DNA fragmentation as a biochemical marker of apoptosis confirmed by TUNEL reaction and agarose gel electrophoresis in human neuroblastoma SK-N-BE(2) and rat glioma C6Bu-1 cells During apoptosis by G-Rh2, protein kinase C (PKC) isoforms were analysed by immunoblotting. In SK-N-BE(2) cells, the levels of a, p and ${\gamma}$ subtypes were increased by undergoing apoptosis, while PKC e isoform increased early in treatment (3 h and 6 h). In addition, PKC s isoform gradually decreased during apoptosis by G-Rh2 and PKC $\theta$ isoform was detected in neither untreated- nor G-Rh1-treated SK-N-BE(2) cells (data not shown). However, no significant changes in the level of S and s isoforms were observed in C6Bu-1 cells undergoing apoptosis by G-Rh2. These results suggest that PKC subtypes may play differential roles in apoptotic signal pathways and their roles can be cell type-specific in apoptosis induced by G-Rh2.

• Journal of Microbiology and Biotechnology
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• v.31 no.12
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• pp.1667-1671
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• 2021

A new homocysteine thiolactone derivative, thiolactomide (1), was isolated along with a known compound, N-acetyl homocysteine thiolactone (2), from a culture extract of soil-derived Streptomyces sp. RK88-1441. The structures of these compounds were elucidated by detailed NMR and MS spectroscopic analyses with literature study. In addition, biological evaluation studies revealed that compounds 1 and 2 both exert neuroprotective activity against 6-hydroxydopamine (6-OHDA)-mediated neurotoxicity by blocking the generation of hydrogen peroxide in neuroblastoma SH-SY5Y cells.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.325-331
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• 2003

3-Nitropropionic acid (3-NP) inhibits electron transport in mitochondria, leading to a metabolic failure. In order to elucidate the mechanism underlying this toxicity, we examined a few biochemical changes possibly involved in the process, such as metabolic inhibition, generation of reactive oxygen species (ROS), DNA strand breakage, and activation of Poly(ADP-ribose) polymerase (PARP). Exposure of SK-N-BE(2)C neuroblastoma cells to 3-NP for 48 h caused actual cell death, while inhibition of mitochondrial function was readily observed when exposed for 24 h to low concentrations (0.2${\sim}$2 mM) of 3-NP. The earliest biochemical change detected with low concentration of 3-NP was an accumulation of ROS (4 h after 3-NP exposure) followed by degradation of DNA. PARP activation by damaged DNA was also detectable, but at a later time. The accumulation of ROS and DNA strand breakage were suppressed by the addition of glutathione or N-acetyl-L-cysteine (NAC), which also partially restored mitochondrial function and cell viability. In addition, inhibition of PARP also reduced the 3-NP-induced DNA strand breakage and cytotoxicity. These results suggest that oxidative stress and activation of PARP are the major factors in 3-NP-induced cytotoxicity, and that the inhibition of these factors may be useful in protecting neuroblastoma cells from 3-NP-induced toxicity.

• Radiation Oncology Journal
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• v.18 no.3
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• pp.177-181
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• 2000

Purpose : Rarity of olfactory neuroblastoma makes it difficult for treating Physician to Practice with a consistent protocol. This study is peformed to analyze our experience with various treatment modalities for patients with olfactory neuroblastoma. Discussion includes review of some recently published literatures. Methods and Materials : Between June of 1979 and April of 1997, 20 patients were treated under the diagnosis of olfactory neuroblastoma at Seoul National University Hospital. There were 14 male and 6 female patients. Age at initial treatment ranged from l3 to 77 years with median or 24 years. fifteen or 20 patients had Kadish stage C. They were treated with various combinations of surgery, radiation therapy and chemotherapy; surgery+postoperative radiation therapy+adjuvant chemotherapy for 2 patients, surgery+postoperative radiation therapy for 6, neoadjuvant chemotherapy+surgery for 1, surgery+adjuvant chemotherapy for 1, surgery only for 2, neoadiuvant chemotherapy+ radiation therapy for 3, radiation therapy+adjuvant chemotherapy for 1, radiation therapy only for 3, and no treatment for 1 patient. Results : Follow-up ranged from 2 month to 204 months with mean of 39.6 months. The overall 5- and 10-year survival rates are 20% and 10%, respectably. Four patients are alive at the time of data analysis. One of four living patients was treated with radical surgery, postoperative radiation therapy and adjuvant chemotherapy, two patients with radical surgery and postoperative radiation therapy, and one with radical surgery only. Conclusion : Multidisciplinary approach, including radical surgery, pre- or post-operative radiation therapy and chemotherapy, should be addressed at the initial time of diagnosis. Although limited by small number of the patients, this study suggests importance of local treatment modality, especially radical surgery in the treatment of lofactory neuroblastoma.

• Korean Journal of Food Science and Technology
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• v.53 no.6
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• pp.715-721
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• 2021

Cognitive impairment and Alzheimer's disease are serious social problems associated with the rising elderly population in Korea. 1,2,3,4,6-Penta-O-galloyl-β-ᴅ-glucopyranose (PGG) is a gallotannin isolated from medicinal plants such as Rhus chinensis. This study was performed to evaluate the effect of PGG on biomarkers related to cognitive function in human neuroblastoma SK-N-SH cells. Inhibition of acetylcholinesterase (AChE) activity is considered to be one of the main therapeutic strategies. PGG inhibited AChE activity in the test tube as well as in SK-N-SH cells. In addition, PGG induced protein and mRNA expression of brain-derived neurotrophic factor (BDNF), which is a mammalian neurotrophin that plays major roles in the development, maintenance, repair, and survival of neuronal populations. As one of the underlying molecular mechanisms that induce BDNF expression, PGG induced the activation of Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII)-cAMP response element binding protein (CREB) pathway. In conclusion, PGG may be an useful material for improving cognitive function.