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      • KCI등재

        Reduction-responsive release property of egg phosphatidylcholine liposomes incorporating benzyl disulfide

        Huangying Guo,김진철 한국공업화학회 2016 Journal of Industrial and Engineering Chemistry Vol.44 No.-

        Reduction-responsive liposome was prepared by incorporating benzyl disulfide in egg phosphatidylcholine(egg PC) liposomal bilayer. Thefluorescence quenching degree of calcein enveloped in egg PCliposome bearing benzyl disulfide decreased from 62.7% to 49.2% and the mean hydrodynamic diameterof the liposome decreased from 276 nm to 206 nm when the egg PC to benzyl disulfide weight ratioincreased from 20:0 to 20:10. The liposomes bearing benzyl disulfide were multi-lamellar vesicles onTEM photos. It was confirmed by Raman spectroscopy that benzyl disulfide was loaded in the liposomalbilayer. The release degree of calcein enveloped in liposome incorporating benzyl disulfide wasinvestigated for 24 h at 25 C, 37 C, and 45 C, when the concentration of DL-dithiothreitol (DTT) was0 mM, 5 mM, 10 mM and 30 mM. At all the DTT concentrations tested, the release degree was moreextensive as the temperature was higher. At all the temperatures tested, the release degree became moreextensive as the DTT concentration increased. For example, the maximum release degree at 37 C ofcalcein loaded in liposome of which egg PC to benzyl disulfide weight ratio was 20:5 increased from 2.9%to 14.8% when DTT concentration increased from 0 mM to 10 mM. DTT could reduce benzyl disulfide tobenzyl thiols and the fragments of benzyl disulfide would re-orient due to its polarity change in theliposomal membrane, resulting in the membranefluctuation and the promoted release. At all thetemperatures and all the DTT concentrations tested, the release was more sensitive to the DTTconcentration as the benzyl disulfide content in liposome was higher, indicating that the reduction of thedisulfide compound was responsible for the promoted release.

      • KCI등재

        Preparation of calcium chloride-loaded solid lipid particles and heat-triggered calcium ion release

        Huangying Guo,김진철 한국화학공학회 2015 Korean Journal of Chemical Engineering Vol.32 No.8

        CaCl2-loaded solid lipid particles (SLPs) were prepared by a melt/emulsification/solidification method. CaCl2 microparticles (1-5 μm) could be obtained in a mortar with aid of the dispersant (Tween 80/Span80 (35/65, w/w)) when the ratio of CaCl2 to dispersant was 2 : 0.1 (w/w). SLP was prepared by dispersing 0.42 g of micronized CaCl2 particles in 2 g of molten PBSA, emulsifying the mixture at 85 oC in 40 ml of Tween 20 solution (0.5% w/v), and quenching the emulsion in an ice bath. The diameter of CaCl2-loaded SLP was 10-150 μm. The unenveloped CaCl2 could be removed by dialysis and the specific loading of CaCl2 in SLP was 0.036mg/mg. An EDS spectrum of CaCl2-loaded SLP, which was dialyzed, showed that the unenveloped CaCl2 was completely removed. Any excipients (dispersant, Tween 20, CaCl2) had little effect on the melting point of SLPs. No appreciable amount of Ca2+ was released in 20-50 oC for 22 h. But the release degree at 60 oC was significant (about 2.3%) during the same period. The matrix of the lipid particle was in a liquid state at 60 oC, so CaCl2 particles could move freely and contact the surrounding water, leading to the release. At 70 oC, the release degree at a given time was a few times higher than that obtained at 60 oC.

      • SCISCIE
      • SCISCIE

        Reduction-responsive vesicles composed of dimethylaminopropyl octadecanamide and dithiodipropionic acid

        Guo, Huangying,Kim, Jin-Chul MARCEL DEKKER JOURNALS 2017 JOURNAL OF DISPERSION SCIENCE AND TECHNOLOGY Vol.38 No.11

        <P>Reduction-responsive vesicle was prepared by salt-bridging N-[3-(dimethylamino)propyl]-octadecanamide (DMAPODA, a cationic amphiphile) using 3,3-dithiodipropionic acid (DTPA, a disulfide diacid compound). According to the transmission electron micrograph and the fluorescence quenching degree (53.2%), it could be said that vesicles were formed when the DMAPODA to DTPA molar ratio was 2:2. The DMAPODA/DTPA associate was considered to be a building block for vesicle formation because DTPA could electrostatically associate with DMAPODA and help the cationic amphiphile assemble into the vesicle. On a differential scanning calorimetric thermogram, the DMAPODA/DTPA vesicle showed two endothermic peaks at 50.6 degrees C and 63.2 degrees C. The peak found at the lower temperature was possibly due to the solid gel-to-liquid crystal phase transition of the vesicular membrane and the peak found at the higher temperature was considered to be due to the melting of DMAPODA, indicating that unassociated DMAPODA coexisted with DMAPODA/DTPA vesicles. The release of calcein enveloped in the vesicle was promoted by DL-dithiothreitol, possibly because DTPA can be broken by the reducing agent to form mercaptopropionic acids and the vesicle could be disintegrated and/or the vesicular membrane would become defective.</P>

      • SCIESCOPUSKCI등재

        Nanoparticle Realgar Powders Induce Apoptosis in U937 Cells through Caspase MAPK and Mitochondrial Pathways

        Wang, Xiao-bo,Gao, Hui-Yuan,Hou, Bai-ling,Huangi, Jian,Xi, Rong-gang,Wu, Li-Jun 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.5

        School of Traditional Chinese Medicines, Shenyang Pharmaceutical University , Department of Pharmacy, Department of traditional Chinese MeNanoparticle realqar powders (NRP) inhibited U937 cell growth in a time and dose-dependent manner. U937 cells treated with NRP showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. Caspase family inhibitor (z-VAD-fmk), caspase-8, -9 inhibitor (z-IETD-fmk, Ac-LEHD-CHO, respectively) and caspase-3 inhibiter (z-DEVD-fmk) partially prevented NRP -induced apoptosis. Moreover, the classical substrates of caspase-3 poly-ADP ribose polymerase (PARP) was degraded after U937 cells treatment with NRP. In audition, NRP Increased the ratio of Bax/Bcl-2 protein expression. Although p38 inhibitor (SB203580) and ERK inhibitor (PD98059) failed to block cell death, JNK inhibitor(SP600125) had marked inhibitory effects on NRP -induced apoptosis. Furthermore, the phosphorylation of JNK was up-regulated, suggesting that JNK was responsible for NRP -induced apoptosis in U937 cells. These results suggested that the caspase, mitochondria and MAPK signal pathways were involved in NRP-induced U937 apoptosis.

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