• Toxicological Research
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• 제32권3호
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• pp.239-243
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• 2016

Propolis is a multicomponent, active, complex resinous substance collected by honeybees from a variety of plant sources. We have studied the effect of propolis on neurite outgrowth of SH-SY5Y human neuroblastoma cells induced to differentiate by all-trans-retinoic acid (RA). Propolis, at a concentration of $3{\mu}g/mL$, had no significant effect on the viability of differentiating SH-SY5Y cells. However, the neurite outgrowth of the differentiating SH-SY5Y cells treated with propolis ($0.3{\sim}3{\mu}g/mL$) for 48 hr was significantly inhibited in a dose-dependent manner. Treatment of RA-stimulated differentiating SH-SY5Y cells with 0.3 to $3{\mu}g/mL$ propolis resulted in decreased level of transglutaminase and 43-kDa growth-associated protein (GAP-43) in a dose-dependent manner. The results indicate that propolis is able to inhibit neurite outgrowth of differentiating SH-SY5Y cells.

• 대한본초학회지
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• 제21권4호
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• pp.85-92
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• 2006

Objectives : To evaluate the neuroprotective effects of added Bo-Yang-Hwan-Oh-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in SH-SY5Y neuronal cells. Methods : To study the cytotoxic effects of BHT on SH-SY5Y cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, SH-SY5Y cells were induced oxidative damages by $H_2O_2$ and then assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effect of BHT by tube test. Results : In MTT assay, $1000{\mu}g/ml$ of BHT was not showed the cytotoxic effect on SH-SY5Y cells. BHT protected SHSY5Y cells from $H_2O_2-induced $ neuronal cell death in a dose-dependent manner. BHT also protected SH-SY5Y cells from $H_2O_2-induced$ DNA fragmentation. BHT effectively scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong antioxidant effects through the free radical scavenging and neuroprotective effects in human neuronal cells.

• Biomolecules & Therapeutics
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• 제20권3호
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• pp.286-292
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• 2012

All-trans retinoic acid (ATRA) is currently used in adjuvant differentiation-based treatment of residual or relapsed neuroblastoma (NB). It has been reported that short-term ATRA treatment induces migration and invasion of SH-SY5Y via transglutaminase-2 (Tgase-2). However, the detailed mechanism of Tgase-2's involvement in NB cell invasion remains unclear. Therefore we investigated the role of Tgase-2 in invasion of NB cells using SH-SY5Y cells. ATRA dose-dependently induced the invasion of SH-SY5Y cells. Cystamine (CTM), a well known tgase inhibitor suppressed the ATRA-induced invasion of SH-SY5Y cells in a dose-dependent manner. Matrix metalloproteinase -9 (MMP-9) and MMP-2, well known genes involved in invasion of cancer cells were induced in the ATRA-induced invasion of the SH-SH5Y cells. Treatment of CTM suppressed the MMP-9 and MMP-2 enzyme activities in the ATRA-induced invasion of the SH-SY5Y cells. To confirm the involvement of Tgase-2, gene silencing of Tgase-2 was performed in the ATRA-induced invasion of the SH-SH5Y cells. The siRNA of Tgase-2 suppressed the MMP-9 and MMP-2 activity of the SH-SY5Y cells. MMP-2 and MMP-9 are well known target genes of NF-${\kappa}B$. Therefore the relationship of Tgase-2 and NF-${\kappa}B$ in the ATRA-induced invasion of the SH-SY5Y cells was examined using siRNA and CTM. ATRA induced the activation of NF-${\kappa}B$ in the SH-SY5Y cells and CTM suppressed the activation of NF-${\kappa}B$. Gene silencing of Tgase-2 suppressed the MMP expression by ATRA. These results suggested that Tgase-2 might be a new target for controlling the ATRA-induced invasion of NBs.

• 생명과학회지
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• 제20권9호
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• pp.1332-1338
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• 2010

사람 신경모세포종 세포주 SH-SY5Y에서 Fenretinide (FenR)에 의한 GD3합성효소(hST8Sia I)의 발현증가기작을 규명하게 위하여 hST8Sia I의 프로모터 활성을 조사해 본 결과 -1146에서 -646영역에서 FenR에 의한 활성증가를 나타내었다. 또한 부위특이적 변이의 분석은 -731에서 -722영역에 위치한 전사인자 NF-kB 결합부위가 hST8Sia I의 FenR에 의한 활성증가에 중요하게 관여하고 있음을 나타내었다. FenR에 의한 hST8Sia I 유전자의 발현유도에 포함된 신호전달기작을 전사인자 단백질의 항체를 이용하여 조사해 본 결과 FenR처리에 의해 세포질에서는 인산화된 AKT단백질 수준의 증가가 관찰되었고 핵내에서는 NF-kB의 p65단백질의 증가가 관찰되었다. 이러한 결과들은 FenR에 의한 hST8Sia I 유전자의 발현증가는 AKT신호전달경로에 의해 활성화된 NF-kB의 핵내로 이동하여 hST8Sia I 유전자의 프로모터에 결합함으로서 전사가 촉진되어 일어난다는 것을 나타낸다.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2020년도 춘계학술대회
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• pp.76-76
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• 2020

Stachys sieboldii Miq. (chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of Stachys sieboldii Miq. (SSM) in cerebral ischemia/reperfusion (I/R) injury is not yet fully understood. In the current study, the neuroblastoma cell line (SH-SY5Y) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate I/R injury in vitro model. The results showed that SSM improved OGD/R-induced inhibitory effect on cell viability of SH-SY5Y Cells. SSM displayed anti-oxidative activity as proved by the decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in OGD/R-induced SH-SY5Y Cells. In addition, cell apoptosis was markedly decreased after SSM treatment in OGD/R-induced SH-SY5Y Cells. The up-regulation of Bcl-2 and down-regulation of Bax, thus reducing the Bax/Bcl-2 ratio that in turn protected the activation of caspase-9 and -3, and inhibition of poly (ADP-ribose) polymerase cleavage, which was associated with the blocking of cytochrome c release to the cytoplasm. Collectively, SSM protected human neuroblastoma SH-SY5Y cells from OGD/R-induced injury via preventing mitochondrial-dependent pathway through scavenging excessive ROS, suggesting that SSM might be a potential agent for the ischemic stroke therapy.

• 대한수의학회지
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• 제54권1호
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• pp.1-6
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• 2014

Parkinson's disease is known to exhibit progressive degeneration of the dopaminergic neurons in the substantia nigra via inhibition of glutathione metabolism. It is well known that 6-Hydroxydopamine (6-OHDA) induces Parkinson's disease-like symptoms, while resveratrol (3,5,4'-trihydroxystilbene) has been shown to have anti-inflammatory and antioxidant effects. In the present study, we investigated the neuroprotective effects of resveratrol, a phytoalexin found in grapes and various plants, on 6-OHDA-induced cell damage to the SH-SY5Y human neuroblastoma cell line. Resveratrol (5 and 10 ${\mu}M$) inhibited 6-OHDA (60 ${\mu}M$)-induced cytotoxicity in SH-SY5Y cells and induced a reduction of the number of apoptotic nuclei caused by 6-OHDA treatment. Additionally, the total apoptotic rate of cells treated with both resveratrol (10 ${\mu}M$) and 6-OHDA (60 ${\mu}M$) was less than that of 6-OHDA treated cells. Resveratrol also dose-dependently (1, 5 and 10 ${\mu}M$) scavenged reactive oxygen species (ROS) induced by 6-OHDA in SH-SY5Y cells and prevented depletion of glutathione in response to the 6-OHDA-induced cytotoxicity in the glutathione assay. Overall, these results indicate that resveratrol exerts a neuroprotective effect against 6-OHDA-induced cytotoxicity of SH-SY5Y cells by scavenging ROS and preserving glutathione.

• 대한한방내과학회지
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• 제35권3호
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• pp.298-308
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• 2014

Objectives: In this study we made an effort to investigate the protective effect of SSMT on the N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) -induced cytotoxicity of SH-SY5Y cells. Methods: The cell viability was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MMT) assay. The fluorescence intensity was measured by using a dye and then with propidium iodide (PI) DNA flow cytometry analysis of the effects on the cell cycle of the SH-SY5Y cells and were used to measure the fluorescence of intracellular reactive oxygen species generation by MPTP. Results: Pretreatment of SSMT significantly suppressed MPTP-induced cytotoxicity, which was revealed as apoptosis characterized by the reduction of cell viability, the increase of ROS production, and the loss of mitochondrial membrane potential in SH-SY5Y cells. Conclusions: These findings suggest that SSMT exerts neuroprotective effects on human neuroblastoma SH-SY5Y cells by MPTP-induced dopaminergic neurodegeneration.

• 대한한방내과학회지
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• 제31권2호
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• pp.254-263
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• 2010

Objectives : The neuroprotective effects of bee venom (BV) have been demonstrated in many studies, but bee venom has many side effects. So we used sweet bee venom (SBV), which has high molecular elements removed to reduce the side effects. I examined the neuroprotective effect of sweet bee venom in 1-methyl-4-phenylpyridine ($MPP^+$)-induced human neuroblastoma SH-SY5Y cells. Methods : To observe the possible toxicity of SBV itself, SH-SY5Y cells were treated with SBV in various concentrations for 3 h and $MPP^+$ in concentrations (1 and 5mM) for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective concentrations of SBV and 1 mM $MPP^+$ for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective of SBV(0.5%), 1 mM $MPP^+$, 5uM AKT inhibitor(LY984002) and 10uM ERK inhibitor(PD98059) for 24 h. The protective effect was measured by cell viability assay. To investigate the degree of apoptosis, caspase-3 enzyme activity was measured in control, $MPP^+$, SBV+$MPP^+$. Results : SBV (0.5%) pretreatment protected the SH-SY5Y cells against $MPP^+$-induced apoptotic cell death. The cell viability was higher in the SH-SY5Y cells that were pretreated with vehicle or nontoxic concentrations of SBV than those not pretreated. The caspase-3 activity was lower in the pretreated groups than these not pretreated. ERK and AKT enzymes have a role in the neuroprotective effects of the sweet bee venom. Conclusions : The results demonstrate that SBV has a protective effect on dopaminergic neurons against $MPP^+$ toxicity. This data suggest that SBV could be a potential therapeutic tool for neurodegenerative diseases such as Parkinson's disease(PD).

• Molecules and Cells
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• 제24권1호
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• pp.105-112
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• 2007

Most neuroblastoma cells have chromosomal aberrations such as gains, losses, amplifications and deletions of DNA. Conventional approaches like fluorescence in situ hybridization (FISH) or metaphase comparative genomic hybridization (CGH) can detect chromosomal aberrations, but their resolution is low. In this study we used array-based comparative genomic hybridization to identify the chromosomal aberrations in human neuroblastoma SH-SY5Y cells. The DNA microarray consisting of 4000 bacterial artificial chromosome (BAC) clones was able to detect chromosomal regions with aberrations. The SH-SY5Y cells showed chromosomal gains in 1q12~ q44 (Chr1:142188905-246084832), 7 (over the whole chro-mosome), 2p25.3~p16.3 (Chr2:18179-47899074), and 17q 21.32~q25.3 (Chr17:42153031-78607159), while chromosomal losses detected were the distal deletion of 1p36.33 (Chr1:552910-563807), 14q21.1~q21.3 (Chr14:37666271-47282550), and 22q13.1~q13.2 (Chr22:36885764-4190 7123). Except for the gain in 17q21 and the loss in 1p36, the other regions of gain or loss in SH-SY5Y cells were newly identified.

• 동의생리병리학회지
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• 제25권6호
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• pp.1039-1043
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• 2011

The purpose of this study is to investigate the modulatory effect of emodin on hydrogen peroxide production in human blastoma SH-SY5Y cells induced by the synthetic analog of double-stranded RNA [polyinosinic-polycytidylic acid]. Hydrogen peroxide production was measured by dihydrorhodamine 123 (DHR) assay. Emodin significantly inhibited the polyinosinic-polycytidylic acid (PIC)-induced production of hydrogen peroxide for 0.5, 2, 12, 18, and 24 hr incubation at the concentrations of 5, 10, 25, and 50 uM in SH-SY5Y (P < 0.05) in dose dependent manner. These results suggest that emodin has neuroprotective property related with its inhibition of hydrogen peroxide production in PIC-induced neuronal cells.