• 한국산학기술학회논문지
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• 제14권5호
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• pp.2524-2528
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• 2013

일반적인 독립기포형 경질폴리우레탄 폼을 만들기 위한 formulation으로부터 개방기포형 경질 우레탄 폼을 얻기 위하여 반응성 기포개방제로서 1-butanol 및 12HSA (12-hydroxystearic acid)의 금속염인 Li-12HSA를 첨가제로 사용하여 만들어진 샘플의 물성과 기포개방 특성에 관한 연구를 진행하였다. 4.0 phr의1-butanol을 단독으로 사용할 때에 비하여 2 phr의 Li-12HSA를 복합하여 사용할 때의 기포개방율은 10.5%에서 98.0%로 현저한 개선효과를 나타내었다. 연구의 결과로서, 반응에 의하여 부피가 큰 막대형 분자를 우레탄 측쇄로 도입함으로서 독립기포형 경질 우레탄 폼의 기포크기나 밀도, 및 열전도율 등의 큰 변화없이 완전 개방기포형 경질 우레탄 폼을 얻을 수 있음을 보여주었다.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.297.3-298
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• 2002

A benzopyranyl derivative. KR32000. synthesized as a plausible KATP opener. has been shown to exert cardioprotective effect in vivo myocardial infarct model. In this study. we investigated whether KR32000 can produce cardioprotective effect against hypoxia- and reactive oxygen species(ROS)-induced injury in heart-derived H9c2 cells. Hypoxic injury was induced by incubating cells in anaerobic chamber (glucose-free. serum-free DMEM. 85% N2. 5% CO2. 10% H2) and oxidative stress was induced by buthionine sulfoximine(BSO). (omitted)

• Archives of Pharmacal Research
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• 제28권12호
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• pp.1358-1364
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• 2005

In this study, we investigated whether a novel anti-ischemic $K_{ATP}$ opener KR-31378 [(2S,3S,4R)­N'-cyano-N-(6-amino-3,4-dihydro-3-hydroxy-2 -methly-2-dimethoxymethly-2H-benzopyran-4-yl)­N'-benzylguanidine] has protective effect against oxidative stress-induced death in heart-derived H9c2 cells. Cell death was induced by BSO, butionine sulfoximine, which inhibits GSH synthesis and subsequently increases reactive oxygen species (ROS) level. Cell death was quantitatively determined by measuring lactate dehydrogenase (LDH) activity and stained by Hoechst 33258. BSO-induced ROS production and mitochondrial membrane potential (MMP) were measured using 2',7'-dichlorofluorescein diacetate oxidation and rhodamine 123, respectively. Both the LDH release and the ROS elevation induced by treatment of H9c2 cells with 10 mM BSO, were significantly decreased by KR-31378. These protective effect and antioxidant effect of KR-31378 appeared to be independent on $K_{ATP}$ channel opening. Cells exposed to BSO showed an early reduction in MMP, and this reduction in MMP was significantly reversed by treatment with KR-31378. Caspase-3 activity in BSO treated H9c2 cells was remarkably increased, and this increased caspase-3 activity was significantly reversed by KR-31378. In conclusion, our results suggest that KR-31378 can produce cardioprotective effect against oxidative stress-induced cell death through antioxidant mechanism.