• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.21
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• pp.9445-9451
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• 2014

Neuroblastoma is the most common extracranial solid tumor in children. Approximately half of the affected patients are diagnosed with high-risk poor prognosis disease, and novel therapies are needed. Sanguinarine is a benzophenanthridine alkaloid which has anti-microbial, anti-oxidant and anti-inflammatory properties. The aim of this study is whether sanguinarine has in vitro apoptotic effects and which apoptotic genes might be affected in the human neuroblastoma cell lines SH-SY5Y (N-myc negative), Kelly (N-myc positive, ALK positive), and SK-N-BE(2). Cell viability was analysed with WST-1 and apoptotic cell death rates were determined using TUNEL. After RNA isolation and cDNA conversion, expression of 84 custom array genes of apoptosis was determined. Sanguinarine caused cell death in a dose dependent manner in all neuroblastoma cell lines except SK-N-BE(2) with rates of 18% in SH-SY5Y and 21% in Kelly human neuroblastoma cells. Cisplatin caused similar apoptotic cell death rates of 16% in SH-SY5Y and 23% in Kelly cells and sanguinarine-cisplatin combinations caused the same rates (18% and 20%). Sanguinarine treatment did not affect apoptototic gene expression but decreased levels of anti-apoptotic genes NOL3 and BCL2L2 in SH-SY5Y cells. Caspase and TNF related gene expression was affected by the sanguinarine-cisplatin combination in SH-SY5Y cells. The expression of regulation of apoptotic genes were increased with sanguinarine treatment in Kelly cells. From these results, we conclude that sanguinarine is a candidate agent against neuroblastoma.

• Journal of Ginseng Research
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• v.34 no.2
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• pp.138-144
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• 2010

Ginseng (Panax ginseng C.A. Meyer) has been shown to have anti-stress effects in animal studies. However, most studies have only managed to detect altered levels of biomarkers or enzymes in blood or tissue, and the actual molecular mechanisms by which ginseng exerts these effects remain unknown. In this study, the anti-oxidative effect of Korean red ginseng (KRG) was examined in human SK-N-SH neuroblastoma cells. Incubation of SK-N-SH cells with the oxidative stressor hydrogen peroxide resulted in significant induction of cell death. In contrast, pre-treatment of cells with KRG decreased cell death significantly. To elucidate underlying mechanisms by which KRG inhibited cell death, the expression of apoptosis-related proteins was examined by Western blot analysis. KRG pre-treatment decreased the expression of the pro-apoptotic gene caspase-3, whereas it increased expression of the anti-apoptotic gene Bcl-2. Consistent with this, immunoblot analysis showed that pre-treatment of the SK-N-SH cells with KRG inhibited expression of the pro-inflammatory gene cyclooxygenase 2 (COX-2). RT-PCR analysis revealed that the repression of COX-2 expression by KRG pre-treatment occurred at the mRNA level. Taken together, our data indicate that KRG can protect against oxidative stress-induced neuronal cell death by repressing genes that mediate apoptosis and inflammation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.1
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• pp.139-145
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• 2005

This study was performed to investigate the effect of Bohyulanshin-tang on brain-derived neurotophic factor(BDNF) expression in SK-N-SH (immortalized human neuroblastoma) cell line. MTT-based cytotoxicity assay revealed that cells of 0.1 mg/ml group and 1 mg/ml group significantly increased compared with Control group. Westren blotting and RT-PCR analysis showed that Bohyulanshin-tang significantly increased BDNF mRNA expression of 0.1 mg/ml group and 1 mg/ml group compared with Control group. Another analysis revealed that Bohyulanshin-tang significantly increased BDNF expression of 0.1 mg/ml group and 1 mg/ml group compared with Control group. These results showed that cell-protective abilities and cell-proliferating effects of Bohyulanshin-tang approached that of Fluoxetine.

• Molecules and Cells
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• v.43 no.4
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• pp.340-349
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• 2020

Oleoylethanolamide (OEA), a bioactive lipid in bone, is known as an endogenous ligand for G protein-coupled receptor 119 (GPR119). Here, we explored the effects of OEA on osteoclast differentiation, function, and survival. While OEA inhibits osteoclast resorptive function by disrupting actin cytoskeleton, it does not affect receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation. OEA attenuates osteoclast spreading, blocks actin ring formation, and eventually impairs bone resorption. Mechanistically, OEA inhibits Rac activation in response to macrophage colony-stimulating factor (M-CSF), but not RANKL. Furthermore, the OEA-mediated cytoskeletal disorganization is abrogated by GPR119 knockdown using small hairpin RNA (shRNA), indicating that GPR119 is pivotal for osteoclast cytoskeletal organization. In addition, OEA induces apoptosis in both control and GPR119 shRNA-transduced osteoclasts, suggesting that GPR119 is not required for osteoclast apoptosis. Collectively, our findings reveal that OEA has inhibitory effects on osteoclast function and survival of mature osteoclasts via GPR119-dependent and GPR119-independent pathways, respectively.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.1
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• pp.15-20
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• 2010

It has been shown that CA repeats in the 3'-untranslated region (UTR) of bcl-2 mRNA contribute the constitutive decay of bcl-2 mRNA and that hnRNP L (heterogenous nuclear ribonucleoprotein L) interacts with CA repeats in the 3'-UTR of bcl-2 mRNA, both in vitro and in vivo. The aim of this study was to determine whether the alteration of hnRNP L affects the stability of bcl-2 mRNA in vivo. Human breast carcinoma MCF-7 cells were transfected with hnRNP L-specific shRNA or hnRNP L-expressing vector to decrease or increase hnRNP L levels, respectively, followed by an actinomycin D chase. An RT-PCR analysis showed that the rate of degradation of endogenous bcl-2 mRNA was not affected by the decrease or increase in the hnRNP L levels. Furthermore, during apoptosis or autophagy, in which bcl-2 expression has been reported to decrease, no difference in the degradation of bcl-2 mRNA was observed between control and hnRNP L-knock down MCF-7 Cells. On the other hand, the levels of AUF-1 and nucleolin, transacting factors for ARE in the 3'UTR of bcl-2 mRNA, were not significantly affected by the decrease in hnRNP L, suggesting that a disturbance in the quantitative balance between these transacting factors is not likely to interfere with the effect of hnRNP L. Collectively, the findings indicate that the decay of bcl-2 mRNA does not appear to be directly controlled by hnRNP L in vivo.

• Journal of Pharmacopuncture
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• v.25 no.3
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• pp.216-223
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• 2022

Objectives: Oxidative stress plays a key role in chronic and acute brain disorders and neuronal damage associated with Alzheimer disease (AD) and other neurodegeneration symptoms. The neuroprotective effects of berberine and Berberis vulgaris (barberry) root extract against apoptosis induced by hydrogen peroxide (H₂O₂) in the human SH-SY5Y cell line were studied. Methods: The methanolic extraction of barberry root was performed using a maceration procedure. Oxidative stress was induced in SH-SY5Y cells by H₂O₂, and an MTT assay was applied to evaluate the neuroprotective effects of berberine and barberry root extract. The cells were pretreated with the half maximal inhibitory concentration (IC₅₀) of each compound (including berberine, barberry root extract, and H₂O₂), and the anti-apoptotic effects of all components were investigated using RT-PCR. Results: The SH-SY5Y cell viability increased in both groups exposed to 75 and 150 ppm barberry extract compared with that in the H₂O₂-treated group. The data showed that exposing SH-SY5Y cells to 30 ppm berberine significantly increased the cell viability compared with the H₂O₂-treated group; treatment with 150 and 300 ppm berberine and H₂O₂ significantly decreased the SH-SY5Y cell viability and was associated with berberine cytotoxicity. The mRNA levels of Bax decreased significantly under treatment with berberine at 30 ppm compared with the control group. A significant increase in Bcl-2 expression was observed only after treatment with the IC₅₀ of berberine. The expression level of Bcl-2 in cells exposed to both berberine and barberry extracts was also significantly higher than that in cells exposed to H₂O₂. Conclusion: The outcomes of this study suggest that treatment of SH-SY5Y cells with barberry extract and berberine could suppress apoptosis by regulating the actions of Bcl-2 family members.

• Journal of Life Science
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• v.20 no.7
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• pp.1054-1065
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• 2010

SH21B is a natural composition composed of seven herbs: Scutellaria baicalensis Georgi, Prunus armeniaca Maxim, Ephedra sinica Stapf, Acorus gramineus Soland, Typha orientalis Presl, Polygala tenuifolia Willd and Nelumbo nucifera Gaertner (Ratio 3:3:3:3:3:2:2). In our previous study, we reported that SH21B inhibited adipogenesis and fat accumulation in 3T3-L1 cells through modulation of various regulators in the adipogenesis pathway. The aim of this study was to analyze the transcriptome profiles for the anti-adipogenic effects of SH21B in 3T3-L1 cells. Total RNAs from SH21B-treated 3T3-L1 cells were reverse-transcribed into cDNAs and hybridized to Affymetrix Mouse Gene 1.0 ST array. From microarray analyses, we identified 2,568 genes of which expressions were changed more than two-fold by SH21B, and the clustering analyses of these genes resulted in 9 clusters. Three clusters among the 9 showed down-regulation by SH21B (cluster 4, cluster 6 and cluster 9), and two clusters showed up-regulation by SH21B (cluster 7 and cluster 8) during the adipogenesis of 3T3-L1 cells. It was found that many genes related to cell proliferation and adipogenesis were included in these clusters. Clusters 4, 6 and 9 included genes which were related with adipogenesis induction and cell cycle arrest. Clusters 7 and 8 included genes related to cell proliferation as well as adipogenesis inhibition. These results suggest that the mechanisms of the anti-adipogenic effects of SH21B may be the modulation of genes involved in cell proliferation and adipogenesis.

• Journal of Korean Biological Nursing Science
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• v.22 no.4
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• pp.223-231
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• 2020

Purpose: The purpose of this study was to investigate the effects of taro extract on brain resilience in in vitro Parkinson's disease model induced by 6-hydroxydopamine (6-OHDA). Methods: To induce a neuroinflammatory reaction and the in vitro Parkinson's disease model, SH-SY5Y cells were stimulated with lipopolysaccharide (LPS) and 6-OHDA, respectively. After that, cells were treated with at various concentrations (1, 5, and 10 mg/mL) of taro extract. Then nitric oxide (NO) production, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, synaptophysin (SYP) and growth associated protein (GAP)-43 messenger ribonucleic acid (mRNA) expression level were measured. Results: Taro extract significantly suppressed LPS-induced NO production. Meanwhile, iNOS and IL-6 mRNA expression decreased in a dose-dependent manner. In addition, taro increased the mRNA expression of SYP and GAP-43 mRNA. Conclusion: These findings indicate that taro played an important role in brain resilience by inhibiting neuronal cell death and promoting neurite outgrowth, synaptogenesis, and neural plasticity. The results of this study suggest that taro may contribute to the prevention of neurodegenerative disease and become a new and safe therapeutic strategy for Parkinson's disease.

• Journal of Plant Biotechnology
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• v.30 no.4
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• pp.323-328
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• 2003

Soil salinity is one of the most serious abiotic stresses limiting the productivity of agricultural crops. To cope with salt stress, plants respond with physiological, developmental and biochemical changes, including the synthesis of a number of proteins and the induction of gene expression. Salicornia herbacea is a halophytic plant that grows in salt marshes and on muddy seashores. In order to understand the biochemical and molecular mechanisms of salt tolerance in S. herbacea, we isolated several genes that involved in the salt tolerance by mRNA differential display. Here we report the cloning of a cDNA encoding fructose-1, 6-bisphosphate aldolase, named ShADL, which is 1293 bp long and contains an open reading frame consisted of 359 amino acids with calculated molecular mass of 39 kDa. ShADL protein showed 86％ identity with Arabidopsis and 78％ with aldolase of common ice plant. Northern blot analysis revealed that the transcript of ShADL gene was increased dramatically depending on the NaCl concentrations.