• 한국전기전자재료학회논문지
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• 제22권2호
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• pp.107-113
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• 2009

In order to improve air stability, we proposed a new active layer of an organic TFT by synthesizing P3HT/POSS conjugated polymer. P3HT/POSS OTFTs with the various P3HT/POSS volume ratios were fabricated and characterized. With the P3HT/POSS volume ratio of 1:1, we achieved the field-effect mobilities of ${\sim}1.19{\times}10^{-3}\;cm^2/v{\cdot}sec$ in the saturation region and the current on/off ratio of ${\sim}2.51{\times}10^2$. The resulting current on-off ratio was much higher than that of the P3HT-based OTFTs and resulted from the dramatic decrease of the off-current. Since the off-current can be reduced by preventing oxygen in atmosphere from doping the P3HT/POSS active layers, this new active layer shows its ability to avoid oxygen doping in atmosphere. Therefore, the improvement of the air stability can be achieved by employing the P3HT/POSS active layers.

• 생약학회지
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• 제44권4호
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• pp.379-383
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• 2013

Portulaca oleracea L. is known to have many biological benefits such as anti-oxidant, anti-inflammatory, anti-allergic and anti-tumor. The objective of this study is to explore the neuroprotective effect of P. oleracea L. against glutamate-induced oxidative stress in mouse hippocampal HT22 cells. P. oleracea L. 70% ethanol extract and solvent fractions have the potent neroprotective effects on glutamate-induced nerotoxicity by induced the expression of heme oxygenase (HO)-1 in HT22 cells. Especially, ethyl acetate fraction showed higher protective effect. In HT22 cell, P. oleracea L. treatment with ERK inhibitor (PD98059) and c-JUN N-terminal kinase (JNK) inhibitor (SP600125) reduced P. oleracea L. ethyl acetate fraction induced HO-1 expression and P. oleracea L. ethyl acetate fraction also increased ERK and JNK phosphorylation. Furthermore, we found that treatment of P. oleracea L. caused the nuclear accumulation of Nrf2. In conclusion, the ethyl acetate fraction of 70% ethanol extract of P. oleracea L. significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2, ERK and JNK pathway in mouse hippocampal HT22. Taken together these finding suggest that P. oleracea L. ethyl acetate fraction is good source for taking active compounds and may be a potential therapeutic agent for brain disorder that induced by oxidative stress and neuronal damage.

• Natural Product Sciences
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• 제15권1호
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• pp.32-36
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• 2009

Glutamate causes neurotoxicity through formation of reactive oxygen species and activation of mitogen-activated protein kinase (MAPK) pathways. MAPK phosphatase-1 (MKP-1) is one of the phosphatases responsible for dephosphorylation/deactivation of three MAPK families: the extracellular signal-regulated kinase-1/2 (ERK-1/2), the c-Jun N-terminal kinase-1/2 (JNK-1/2), and the p38 MAPK. In this report, the potential involvement of MKP-1 in neuroprotective effects of curcumin, the active ingredient of turmeric (Curcuma longa), was examined using HT22 cells. Glutamate caused cell death and activation of ERK-1/2 but not p38 MAPK or JNK-1/2. Blockage of ERK-1/2 by its inhibitor protected HT22 cells against glutamate-induced toxicity. Curcumin attenuated glutamate-induced cell death and ERK-1/2 activation. Interestingly, curcumin induced MKP-1 activation. In HT22 cells transiently transfected with small interfering RNA against MKP-1, curcumin failed to inhibit glutamate-induced ERK-1/2 activation and to protect HT22 cells from glutamate-induced toxicity. These results suggest that curcumin can attenuate glutamate-induced neurotoxicity by activating MKP-1 which acts as the negative regulator of ERK-1/2. This novel pathway may contribute to and explain at least one of the neuroprotective actions of curcumin.

• Molecules and Cells
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• 제45권4호
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• pp.216-230
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• 2022

SERTA domain-containing protein 1 (Sertad1) is upregulated in the models of DNA damage and Alzheimer's disease, contributing to neuronal death. However, the role and mechanism of Sertad1 in ischemic/hypoxic neurological injury remain unclear. In the present study, our results showed that the expression of Sertad1 was upregulated in a mouse middle cerebral artery occlusion and reperfusion model and in HT22 cells after oxygen-glucose deprivation/reoxygenation (OGD/R). Sertad1 knockdown significantly ameliorated ischemia-induced brain infarct volume, neurological deficits and neuronal apoptosis. In addition, it significantly ameliorated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Sertad1 knockdown significantly inhibited the ischemic/hypoxic-induced expression of p-Rb, B-Myb, and Bim in vivo and in vitro. However, Sertad1 overexpression significantly exacerbated the OGD/R-induced inhibition of cell viability and apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. In further studies, we demonstrated that Sertad1 directly binds to CDK4 and the CDK4 inhibitor ON123300 restores the effects of Sertad1 overexpression on OGD/R-induced apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. These results suggested that Sertad1 contributed to ischemic/hypoxic neurological injury by activating the CDK4/p-Rb pathway.

• Clinical and Experimental Pediatrics
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• 제52권9호
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• pp.984-990
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• 2009

목 적 : 부당경량아는 소아기 저신장의 주요한 이유 중의 하나이다. 유전적 요소는 부당경량아의 성장에 중요한 영향을 끼친다고 알려져 있다. 일반 소아와 유전적 요소사이의 관계에 대한 몇몇 보고가 있다. 하지만 부당경량아와 유전적 요소사이의 관계에 대한 보고는 많지 않다. 그래서 본 논문에서는 부당경량아의 성장과 부모중간키의 측정에 의한 유전적 요소 사이의 관계에 대해 연구하였다. 그리고 IGF-I, IGFBP-3 그리고 유전적 요소가 반영된 출생 후 성장과의 관계에 대해 연구하였다. 방 법 : 1989년부터 2002년까지 한림의대 강동성심병원에서 태어난 신생아로 출생체중이 10백분위수 미만인 부당 경량아 300명 중 추적 관찰이 가능했던 49명을 대상으로 하였다. 대상아의 부모중간키를 최종 평균값으로 하는 새로운 개인별 교정성장곡선을 구해 해당 연령의 표준편차를 적용하여 cHtSDS를 계산하였다. cHtSDS${\geq}0$ (n=35)인 1군, cHtSDS<0 (n=14)인 2군으로 나누고 두 군 간에 IGF-I과 IGFBP-3를 비교하였다. 결 과 : 1군과 2군의 HtSDS와 cHtSDS는 $0.28{\pm}1.05$, $-0.95{\pm}0.85$ (P=0.000), $0.78{\pm}0.93$, $-0.46{\pm}0.67$ (P=0.000)이었다. 또한 IGF-I SDS는 각각 $2.82{\pm}3.69$, $0.23{\pm}2.42$로 1군이 2군에 비하여 유의하게 더 높았다(P=0.012). 전체 cHtSDS ($0.42{\pm}1.03$)는 HtSDS ($-0.22{\pm}1.10$)보다 더 높았고(P=0.000), cHtSDS는 IGF-I SDS와 유의한 양의 상관관계를 가졌다(P=0.016). 결 론 : 본 연구 결과로 볼 때 cHtSDS는 HtSDS와 유의하게 차이가 났다. 현재의 일률적인 표준성장곡선에 의한 성장평가는 유전적 요소를 제대로 반영하지 못할 수 있다. 진정한 성장상태의 평가는 부모중간키 같은 유전적 요소를 반영한 개인별 교정성장곡선의 사용에 의해 가능할 것이다. 비록 cHtSDS를 계산하는 방법론상의 문제가 아직 있지만, cHtSDS는 부당경량아의 성장평가에 유용한 방법이 될 수 있다.

• Archives of Pharmacal Research
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• 제22권2호
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• pp.113-118
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• 1999

Previous work in our laboratory has shown that the N-methyl-D-aspartate (NMDA) receptor antagonists, AP-5, CPP, MK-801, ketamine, dextrorphan and dextromethorphan cause a pronounced enhancement of 5-hydroxytryptamine (5-HT)-induced head-twitch response (HTR) in intact mice, suggesting the involvement of NMDA receptors in the glutamatergic modulation of serotonergic function at the postsynaptic $5-HT_{2}$ receptors. The purpose of this study was to extend our previous work on the behavioral interaction between glutamatergic and serotonergic receptors. In the present study, both competitive (AP-5 and CPP) and noncompeti-tive (MI-801, ketamine, dextrorphan and dextromethorphan) NMDA receptor antagonists markedly enhanced 5-HT-induced selective serotonergic behavior, HTR, in p-chlorophenylalanine (PCPA)-treated mice which were devoid of any involvement of indirect serotonergic function, to establish the involvement of the NMDA receptor in 5-HT-induced HTR at the postsyaptic $5-HT_{2}$receptors. In addition, the enhancement of 5-HT-induced HTR was inhibited by a dopamine agonist, apomorphine, NMDA receptor antagonist, NMDA and a serotonin $5-HT_{2}$receptor antagonist, cyproheptadine, in PCPA-treated mice. Therefore, the present results support our previous conclusion that the NMDA receptors play an important role in the glutamatergic modulation of serotonergic function at the poststynaptic $5-HT_{2}$ receptors.

• 동의신경정신과학회지
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• 제22권2호
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• pp.147-162
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• 2011

Objectives : This experiment was designed to investigate the effect of the BSGE hot water extract on serotonin biosynthesis of depression model. Methods : The cytotoxicity of the BSGE hot water extract was analyzed by MTT assay on P815 cell. The antioxidant activity was measured by DPPH free radical-scavenging activity and SOD activity on P815 cell. The quantity of 5-HT and expression of TPH-1, AAADC and MAOa mRNA was measured by of HPLC profle Analysis on P815 cell. Results : 1. The BSGE hot water extract increased DPPH free radical-scavenging activity and SOD activity on P815 cell. 2. The BSGE hot water extract increased significantly the quantity of 5-HT. 3. The BSGE hot water extract increased the expression of TPH-1 mRNA. Conclusions : This experiment shows that the BSGE hot water extract might be effective for the prevention and treatment of depression. Investigation into the clinical use of the BSGE hot water extract for depression is suggested for future research.

• 동의생리병리학회지
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• 제25권4호
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• pp.628-634
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• 2011

The roots of Polygala tenuifolia Willd. is a well-known traditional medicine used as expectorant, tonic, tranquilizer in Asia including China and Korea. And also have been used to treat amnesia, neurasthenia, palpitation, insomnia, and disorientation. Glutamate-induced oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemia. Inducible heme oxygenase (HO)-1 acts against oxidants that are thought to play a role in the pathogenesis of these diseases. NNMBS269, acid hydrolysis EtOAc fraction of the P. tenuifolia showed dominant neuroprotective effects on glutamate-induced neurotoxicity in mouse hippocampal HT22 cells while general EtOAc fraction of the P. tenuifolia (NNMBS268) not shown. NNMBS269 induced the expression of HO-1 protein that has been proposed to play an important cellular defense role against oxidant injury. In addition increased HO activity. In mouse hippocampal HT22 cells, NNMBS269 makes the nuclear accumulation of nuclear factor E2-related factor 2 (Nrf2). In conclusion, acid hydrolysis EtOAc fraction the P. enuifolia. (NNMBS269) significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2 translocation in mouse hippocampal HT22 cells.

• 약학회지
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• 제47권2호
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• pp.85-92
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• 2003

Seok-jeong (SJ) is a solution of various metal ions and numerous other organic substances produced through extraction and fermentation of herbs and soil using geo-microbes, and it has been shown to improve symptoms of senile dementia. In this study, we investigated the protective effects of SJ against neurotoxicity of cadmium in HT22 hippocampal neuron cell line. SJ significantly protected from the cadmium-induced decreased cell viability measured by MTT assay (p＜0.01). The protective effects of SJ against cadmium toxicity were confirmed through observing morphological changes using inverted microscope. Additionally, SJ significantly repressed the formation of lipid peroxidation induced by high concentration of cadmium, and likewise, significantly repressed the reduction of glutathione by cadmium in HT22 cells. Vitamin C at the concentration found in SJ did not show any protective effect against cadmium toxicity in HT22 cells, indicating that vitamin C may not have a major role in the protective mechanism of SJ. Taken together, these results suggest that SJ may be a valuable agent for the protection of cadmium toxicity on the neuronal cells, and that the mechanism of the action of SJ may be due to reduced lipid peroxidation and increased glutathione level.

• Biomolecules & Therapeutics
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• 제27권2호
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• pp.145-151
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• 2019

Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.