• 공업화학
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• 제7권1호
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• pp.59-66
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• 1996

양말단에 아미노기가 결합된 일련의 bisamino-PEG($Jeffamine^{(R)}ED$)를 함유한 키토산 비드들을 알칼리 용액을 사용한 capillary extrusion method에 의해 제조하였다. 제조된 각각의 비드들에 대한 swelling kinetics를 조사한 결과, 키토산비드 내부에 PEG 사슬이 길어질수록 팽윤이 늦게 진행되었다. 또한 키토산 비드에 함유된 bisamino-PEG들의 방출현상을 정량적으로 알아 보기 위해 양말단의 1차 아민기에 fluorescamine을 결합시킨 후, UV spectra로 방출과정을 추적하였다. 실험결과 키토산 비드 내부에 있는 PEG 사슬이 길수록 방출시간은 $Jeffamine^{(R)}ED$-600 < $Jeffamine^{(R)}ED$-900 < $Jeffamine^{(R)}ED$-2001 순으로 지연되는 경향을 나타내었다. 이는 PEG 사슬이 길어질수록 키토산과의 수소결합에 의한 상호작용이 강화되고 그 결과 방출기간이 지연된 것으로 사료된다.

• 한국식품영양학회지
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• 제29권6호
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• pp.923-929
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• 2016

The purpose of this study was to evaluate the protective effect of $PineXol^{(R)}$ on $H_2O_2$-induced cell death in SK-N-MC cells, and in early stage focal ischemia rodent model. SK-N-MC cells were pre-treated with $200{\mu}M$ $H_2O_2$ or various concentrations of $PineXol^{(R)}$ (10, 30, and 50 pg/mL) for 24 h, and then exposed to $H_2O_2$ for 3 h. Cell death was assessed by the CCK-8 assay, reactive oxygen species (ROS) assay, and lactate and dehydrogenase (LDH) release assay. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) expressions were also analyzed by western blotting. Focal ischemia rodent model was used as the in vivo model, and different concentrations of $PineXol^{(R)}$ (1, 10, and 100 mg/kg) were administered. One week after administration, reduction of infarct volume was analyzed by TTC staining. Cell viability of $H_2O_2$-treated SK-N-MC cells significantly increased by pre-treatment of $PineXol^{(R)}$ (p<0.05). $PineXol^{(R)}$ pre-treatment also induced significant decrease of ROS and LDH expressions. However, $PineXol^{(R)}$ did not affect the infarct volume. These results suggest that $PineXol^{(R)}$ has significant neuroprotective effect in vitro, but statistical significance was not confirmed in the in vivo focal ischemia model.

• 한국안전학회지
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• 제29권2호
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• pp.24-30
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• 2014

There have been controversies over whether explosion hazardous area(EHA) should be classified for facilities which use lighter-than-air gases such as city gas, hydrogen and ammonia. Two view points are confronting each other: an economic piont of view that these gases are lighter than air and disperse rapidly, hence do not form EHA upon release into the atmosphere, and a safety point of view that they are also inflammable gases, hence can form EHA although the extent is limited compared to heavy gases. But various standards such as KS, IEC, API, NFPA do not exclude light gases when classifying EHA and present examples of EHA for light gas facilities. This study calculates EHA using the hypothetical volume in the IEC code where the hole sizes required for the calculation were selected according to various nominal pipe sizes in such a way to conform to the EHA data in the API code and HSL. Then, 25 leakage scenarios were suggested for 5 different pipe sizes and 5 operating pressures that cover typical operating conditions of light gas facilities. The EHA for the minimum leakage scenario(25 mm pipe, 0.01MPa pressure) was found to correspond to a hypothetical volume larger than 0.1 $m^3$(medium-level ventilation). This confirms the validity of classifying EHA for facilities using lighter-than-air gases. Finally, a computer program called HACPL was developed for easy use by light gas facilities that classifies EHA according to operating pressures and pipe sizes.

• BMB Reports
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• 제46권12호
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• pp.594-599
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• 2013

The anti-inflammatory activity of eriodictyol and its mode of action were investigated. Eriodictyol suppressed tumor necrosis factor (mTNF)-${\alpha}$, inducible nitric oxide synthase (miNOS), interleukin (mIL)-6, macrophage inflammatory protein (mMIP)-1, and mMIP-2 cytokine release in LPS-stimulated macrophages. We found that the anti-inflammatory cascade of eriodictyol is mediated through the Toll-like Receptor (TLR)4/CD14, p38 mitogen-activated protein kinases (MAPK), extracellular-signal-regulated kinase (ERK), Jun-N terminal kinase (JNK), and cyclooxygenase (COX)-2 pathway. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that eriodictyol exhibits good binding affinity to JNK, $8.79{\times}10^5M^{-1}$. Based on a docking study, we propose a model of eriodictyol and JNK binding, in which eriodictyol forms 3 hydrogen bonds with the side chains of Lys55, Met111, and Asp169 in JNK, and in which the hydroxyl groups of the B ring play key roles in binding interactions with JNK. Therefore, eriodictyol may be a potent anti-inflammatory inhibitor of JNK.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Archives of Pharmacal Research
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• 제28권3호
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• pp.311-318
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• 2005

Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC­PK1 cells were treated with H$_2$O$_2$ in the absence of serum to induce cell death. Subsequent to exposure to H$_2$O$_2$, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H202-treated control cells, it was observed that 0.5 $\mu$M of desipramine and 25 $\mu$M of NAC exhibited about 90 and $95\%$ of cytoprotection, respectively, against H$_2$O$_2$-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and $3\%$ respectively, when compared to $71\%$ in H$_2$O$_2$-exposed cells. Cellular glutathione level in 500 $\mu$M H202-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H$_2$O$_2$-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H$_2$O$_2$-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

• Biomaterials and Biomechanics in Bioengineering
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• 제2권1호
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• pp.23-32
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• 2015

Facile immobilization of growth factors in hyaluronic acid (HA) hydrogels using dual enzymes is reported in the paper. The hydrogels were formed by using horseradish peroxidase (HRP) and hydrogen peroxide ($H_2O_2$) and transforming growth factor-${\beta}3$ (TGF-${\beta}3$) was covalently conjugated on the hydrogels in situ using tyrosinase (Ty) without any modifications. For the preparation of hydrogels, HA was grafted with poly(ethylene glycol) (PEG), which was modified with a tyrosine. The gelation times of the HA hydrogels were ranging from 415 to 17 s and the storage moduli was dependent on the concentration of $H_2O_2$ and Ty (470-1600 Pa). A native TGF-${\beta}3$ (200 ng/mL) was readily encapsulated in the HA hydrogels and 17% of the TGF-${\beta}3$ was released over 1 month at the Ty concentration of 0.5 KU/mL, while the release was faster when 0.3 KU/mL of Ty was used for the encapsulation (27%). It can be suggested that the growth factors resident in the hydrogels for a long period of time may lead cells proliferating and differentiating, whereas the growth factors that are initially released from the hydrogels can induce the ingrowth of cells into the matrices. Therefore, the dual enzymatic methods as facile gel forming and loading of various native growth factors or therapeutic proteins could be highly promising for tissue regenerative medicines.

• Elastomers and Composites
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• 제39권1호
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• pp.42-50
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• 2004

본 연구는 열잠재성 개시제인 N-benzylpyrazinium hexafluoroantimonate (BPH)로 개시되어진 이관능성 에폭시인 diglycidylether of bisphenol A (DGEBA)와 변성 polyurethane (PU) 블렌드의 PU의 함량에 따른 경화거동과 파괴인성을 연구하였다. 블렌드의 경화거동은 시차주사 열량계(DSC)와 near-IR 을 통해 관찰하였고, 파괴인성은 임계응력 세기인자($K_{IC}$)와 임계 변형에너지 방출속도($G_{IC}$)를 측정하였다. 실험 결과, 경화 활성화에너지($E_a$)와 전환율(${\alpha}$)은 PU의 함량이 10 phr에서 최고값을 나타냈으며, $K_{IC}$는 전환율과 유사한 경향을 나타냄을 확인하였다. 이는 PU의 이소시아네이트기와 DGEBA의 하이드록실기 사이의 수소 결합이 증가함에 따라 블렌드의 가교밀도가 증가했기 때문으로 판단되어 진다.

• Journal of Radiation Protection and Research
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• 제30권1호
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• pp.45-54
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• 2005

원자력시설로부터 삼중수소 사고 누출시 시설 주변 농작물의 삼중수소 오염 평가를 위한 동적격실모델 ECOREA-H3를 개발하였다. 모델의 격실은 크게 대기, 토양, 농작물로 구성되며 농작물은 엽채류 곡물류, 근군류의 3개 소그룹으로 분류하여 각각 독립적으로 모델링하였다. 벼에 대한 삼중수소 피폭실험 해석을 통해 모델의 예측 정확도가 조사되었다. 모델링 결과 추수시 벼이삭의 TFWT 농도는 입력데이터 중 공기의 절대습도, 뿌리흡수비 강우량에 OBT 농도는 공기의 절대습도, 이삭의 성장기간, 유기물의 수소함량의 영향을 상대적으로 크게 받는 것으로 나타났다. 벼이삭 OBT 농도에 대한 모델 계산과 실험 측정값은 잘 일치하였다.

• The Korean Journal of Physiology and Pharmacology
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• 제8권1호
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• pp.43-50
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• 2004

Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. Amrinone, a specific inhibitor of phosphodiesterase 3, has an antioxidant activity against PMNs. Therefore, we hypothesized that amrinone could attenuate PMNs-Induced cardiac dysfunction by suppression of reactive oxygen species (ROS) produced fby PMNs. In the present study, we examined the effects of amrinone on isolated ischemic (20 min) and reperfused (45 min) rat hearts perfused with PMNs. Amrinone at $25\;{\mu}M$, given to hearts during the first 5 min of reperfusion, significantly improved coronary flow, left ventricular developed pressure (P<0.001), and the maximal rate of development of left ventricular developed pressure (P<0.001), compared with ischemic/reperfused hearts perfused with PMNs in the absence of amrinone. In addition, amrinone significantly reduced myeloperoxidase activity by 50.8%, indicating decreased PMNs infiltration (p< 0.001). Superoxide radical and hydrogen peroxide production were also significantly reduced in fMLP- and PMA-stimulated PMNs pretreated with amrinone. Hydroxyl radical was scavenged by amrinone. fMLP-induced elevation of $[Ca^{2+}]_i$ was also inhibited by amrinone. These results provide evidence that amrinone can significantly attenuate PMN-induced cardiac contractile dysfunction in the ischemic/reperfused rat heart via attenuation of PMNs infiltration into the myocardium and suppression of ROS release by PMNs.