• Biomolecules & Therapeutics
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• 제30권6호
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• pp.570-575
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• 2022

Stress breaks body balance, which can cause diverse physiological disorders and worsen preexisting diseases. However, recent studies have reported that controllable stress and overcoming from stress reinforce resilience to resist against more intense stress afterwards. In this study, we investigated the protective effect of corticosterone (CORT), a representative stress hormone against hydrogen peroxide (H₂O₂)-induced neuronal cell death and its underlying molecular mechanism in SH-SY5Y cells, a human neuroblastoma cell line. The decreased cell viability by H₂O₂ was effectively restored by the pretreatment with low concentration of CORT (0.03 μM for 72 h) in the cells. H₂O₂-increased expression of apoptotic markers such as PUMA and Bim was decreased by CORT pretreatment. Furthermore, pretreatment of CORT attenuated H₂O₂-mediated oxidative damages by upregulation of antioxidant enzymes via activation of nuclear factor erythroid 2-related factor 2 (Nrf2). These findings suggest that low concentration of CORT with eustressed condition enhances intracellular self-defense against H₂O₂-mediated oxidative cell death, suggesting a role of low concentration of CORT as one of key molecules for resilience and neuronal cell survival.

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2003년도 추계국제학술대회
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• pp.177-177
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• 2003

Methylmercury (MeHg) is a well-known neurotoxicant that causes severe damage to the central nervous system in humans. Many reports have shown that MeHg is poisonous to human body through contaminated foods and has released into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established so far. In this study, suppressive subtractive hybridization (SSH) was performed to identify differentially expressed genes on human neuroblastoma cell line, SH-SY5Y treated with DMSO and MeHg (6.25 uM) for 6 hr. Differentially expressed cDNA clones were sequenced and were screened by dot blot to eliminate false positive clones. 13 of 35 screened genes were confirmed using real time RT-PCR. These genes include EB1,90-kDa heat-shock protein, chromosome condensation-related SMC-associated protein and brain peptide Al, etc. Analysis of these genes may provide an insight into the neurotoxic effects of MeHg in human neuronal cells and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.

• 한국동물학회지
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• 제38권4호
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• pp.542-549
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• 1995

Extracellular matrix(ECM) 단백질이 SK-N-SH 및 IMR-32 세포주가 신경계 세포로 분화되는 데 미치는 영향을 조사하였다. Laminin과 collagen으로 도말한 배양기에서 7일간 배양했을 때 SK-N-SH세포는 잘 발달된 신경측색생장을 보였으나 IMR-32세포는 뚜렷한 형태변화를 나타내지 않았다. 왜 IMR-32세포가 ECM 단백질에 반응을 하지 않는가를 규명하기 위하여 ECM단백질에 의한 초기 신호전달기작을 두 세포주에서 분석하였다. ECM 단백질을 도말한 배양기에 세포를 깔았을 때 한시간 만에 tyrosine 인산화된 단백질이 두 세포 모두 증가함을 볼 수 있었다. 아울러 focal adhesion kinase(FAK)의 tyrosine 인산화도 두 세포주 모두에서 증가하였다. 이러한 결과는 두 세포주가 ECM 단백질에 의한 초기 신호전달체계가 정상임을 의미한다. 신경세포 분화과정에 증가한다고 알려진 Bcl-2 및 NSE의 량을 ECM 단백질 처리후 조사하였을 때 SK-N-SH 세포주는 두 단백질이 증가 했지만 IMR-32 세포주는 변화가 없었다. 이러한 결과는 IMR-32 세포주가 ECM 단백질에 반응하지 않는 것이 ECM 단백질에 의한 신호전달체계에 문제가 있다기 보다 신경계세포로 분화되는 데 필요한 유전인자의 발현조절에 문제가 있음을 시사한다.

• Journal of Nutrition and Health
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• 제50권5호
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• pp.415-425
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• 2017

건 여주로부터 얻은 70%에탄올 추출물의 항산화 효과를 측정하고, $H_2O_2$에 의해 유도된 산화적 스트레스에 대한 신경세포 보호효과를 알아보기 위해 human neuroblastoma cell인 SK-N-MC세포를 이용하여 실험을 수행하였다. 여주 추출물의 총 폴리페놀과 플라보노이드 함량은 각각 28.51 mg gallic acid/extract g과 3.95 mg catechin/extract g 이었고, 추출물의 DPPH 라디칼 소거능 ($IC_{50}$)은 $506.95{\mu}g/ml$ 이었다. 여주추출물을 신경세포에 전 처리한 후 $H_2O_2$을 처리하여 산화적 스트레스를 유도했을 때, 여주추출물에 의해 세포생존율은 증가되었고 세포내 ROS는 감소되는 것을 확인하였다. 그리고 세포내 항산화 방어시스템인 항산화효소 (SOD-1,2와 GPx-1)의 mRNA 발현이 여주추출물 처리에 의해 control 수준으로 회복되거나 control 보다 증가되는 결과를 보였으며, ROS 의존적 세포사멸과 연관 있는 것으로 알려진 MAPK pathway 중 p38과 JNK의 인산화를 여주추출물이 억제하였다. 또한 cleaved caspase-3와 cleaved PARP의 발현도 여주추출물의 처리에 의해 감소되었다. 본 연구 결과에서 70% 에탄올 여주추출물은 항산화효능이 우수하여 ROS를 직접적으로 제거할 뿐 아니라 세포내 ROS 축적을 억제시키는 효과를 보여주었다. 그리고 신경세포 내 항산화효소들의 발현 증가 기전과 p38, JNK의 인산화 억제 및 cleaved caspase-3, cleaved PARP의 발현 억제를 통한 세포사멸 억제 기전을 통해 산화적 스트레스로부터 신경세포를 보호하는 효과가 있음을 제시하고 있다. 따라서 여주추출물은 산화적 스트레스에 의한 알츠하이머병이나 파킨슨병 등과 같은 신경변성질환 (neurodegenerative disease)에 대한 예방 및 치료제의 소재로써 이용가치가 충분한 것으로 사료된다.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1996년도 한국생물과학협회 국제학술대회
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• pp.224.2-224
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• 1996

No Abstract, See Full Text

• 한국약용작물학회:학술대회논문집
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• 한국약용작물학회 2008년도 춘계학술발표회
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• pp.186-187
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• 2008

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.182.1-182.1
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• 2003

Occupational exposure to cadmium (Cd) can result in brain disorders and olfactory dysfunction is the most well-known symptom. Recently Cd has been shown to induce apoptosis by activating MAPKs in various cell types. However, intracellular signaling pathways of Cd-induced cytotoxicity in neuronal cells is not known well. Thus, in the present study, we studied role of JNK and its well-known downstream transcription factor, c-JUN, in Cd-induced neuronal cell death. (omitted)

• Archives of Pharmacal Research
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• 제23권5호
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• pp.518-524
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• 2000

We examined the modulation of protein kinase C (PKC) subtypes during apoptosis induced by ginsenoside Rh2 (G-Rh2) in human neuroblastoma SK-N-Bl(2) and rat glioma C6Bu-1 cells. Apoptosis induced by C-Rh2 in both cell lines was confirmed, as indicated by DNA fragmentation and in situ strand breaks, and characteristic morphological changes. During apoptosis induced by G-Rh2 in SK-N-BE(2) cells, PKC subtypes $\alpha$, $\beta$ and $\gamma$ were progressively increased with prolonged treatment, whereas PKC $\delta$ increased transiently at 3 and 6 h and PKC $\varepsilon$ was gradually down-regulated after 6 h following the treatment. On the other hand, PKC subtype $\beta$ markedly increased at 24 h when maximal apoptosis was achieved. In C6Bu-l cells, no significant changes in PKC subtypes $\alpha$, $\gamma$, $\delta$, $\varepsilon$ and $\beta$ were observed during apoptosis induced by G-Rh2. These results suggest the evidence for a possible role of PKC subtype in apoptosis induced by G-Rh2 in SK-N-BE(2) cells but not in C6Bu-1 cells, and raise the possibility that G-Rh2 may induce apoptosis via different pathways interacting with or without PKC in different cell types.

• The Korean Journal of Physiology
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• 제29권2호
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• pp.301-307
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• 1995

To explore electrophysiological properties of the ${\delta}-Opioid$ receptors artificially expressed in the mammalian cell, effect of an opioid agonist DPDPE $(1\;{\mu}M)$ on the voltage-sensitive outward currents was examined in the HEK293 (human embryonic kidney) cells transfected with ${\delta}-Opioid$ receptor cDNA cloned from NG-108-15 $(neuroblastoma\;{\times}\;glioma\;hybrid)$ cDNA library. Also studied were effects of 8-bromo-cyclic AMP and naloxone on DPDPE-induced changes in the voltage sensitive outward current. The voltage sensitive outward currents were recorded using perforated patch technique at room temperature. In the non-transformed HEK293 cells, DPDPE did not alter voltage sensitive outward current, indicating that no native ${\delta}-Opioid$ receptor had been developed. However, $(1\;{\mu}M)$ DPDPE remarkably increased the voltage sensitive outward current in the transformed HEK293 cells. The increment in voltage sensitive outward current peaked in $7{\sim}10\;minutes$ after DPDPE application, and the maximum DPDPE-activated outward current $(313.1{\pm}12.3\;pA)$ was recorded when the membrane potential was depolarized to +70mv. Following pretreatment of the transformed HEK293 cells with 1 mM 8-bromo-cyclic AMP, DPDPE failed to increase the voltage sensitive outward currents. On the other hand, naloxone completely abolished DPDPE-activated voltage sensitive outward current in the transformed HEK293 cells. The results of present study suggest that in the transformed HEK293 cells an activation of the ${\delta}-Opioid$ receptors by an opioid agonist DPDPE increases the voltage-sensitive potassium current as a result of decrement in cyclic AMP level.

• Preventive Nutrition and Food Science
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• 제10권4호
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• pp.353-356
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• 2005

It has been recently reported that boron affects bone metabolism in humans and animals. In this study we examined whether boron affects the proliferation on various cell types, MG-63, HOS, Raw 264.7 and SK-N-SH. When treated with different concentrations of boron $(1,\;10,\;100{\mu}M)$ for 24 and 48 hr, the proliferation of MG-63 cells was enhanced at $10{\mu}M\;(p<0.05)$, for 24 hr. In HOS cells, boron had no effect on cell proliferation at 24 or 48 hr. In addition, treatment of pre-osteoclastic cells (Raw 264.7) with 1, 10, $100{\mu}M$ boron resulted in no effect on cell proliferation. Proliferation of neuronal cells (SK-N-SH) was enhanced by boron in a concentration dependent manner at low concentrations (0.1, 0.5, $1{\mu}M$). Besides proliferation activity, boron has an effect on the enhancement of NO production in SK-N-SH cells in a concentration-dependent manner. These studies showed that boron enhances proliferation of osteoblastic cells (especially MG-63), depending upon the concentration of boron. These results also provide further evidence of the positive effects of boron in neuronal disease.