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윤주병,황성호,김동국,강성구,최진호,Yun, Ju Byeong,Hwang, Seong Ho,Kim, Dong Guk,Gang, Seong Gu,Choe, Jin Ho Korean Chemical Society 2000 Bulletin of the Korean Chemical Society Vol.21 No.3
The cerium ion intercalated aluminosilicate was prepared by ion exchange reaction between $Na^+$ in montmorillonite and $Ce^{+4}$ in aqueous solution. The X-ray absorption near edge structrure(XANES) analyses indicate that the $Ce^{+4}$ ions are partially reduced to the $Ce^{+3}$ ones during the intercalation into layered aluminosilicate due to a charge transfer between host and intercalant. From the EXAFS analysis, two different (Ce-O) bonding pairs could be characterized with the distances and coordination numbers of 2.31 $({\pm}0.02){\AA}$ ${\times}$ 8.2 $({\pm}1.5)$ and 2.66 $({\pm}0.02){\AA}$ ${\times}$ 2.7 $({\pm}1.0)$, respectively, with the oxygen atoms as the first nearest neighbor, and two (Ce-Ce) pairs at 3.78 ${\AA}$ as the second neighbor. It is therefore concluded that the most probable Ce-species stabilized in the interlayer space of aluminosilicate after the intercalation is the tetrameric Ce-polyoxy/hydorxy cations with the mixed valent state of 0.75 $Ce^{+4}$.0.25 $Ce^{+3}$.
Trimeric Chromium Oxyformate Route to Chromia-Pillared Clay
윤주병,황성호,최진호,Yun, Ju Byeong,Hwang, Seong Ho,Choe, Jin Ho Korean Chemical Society 2000 Bulletin of the Korean Chemical Society Vol.21 No.10
A chromia-pillared clay has been prepared by ion exchange type intercalation reaction between the sodium ion in montmorillonite and the trimeric chromium oxyformate (TCF) ion, and by subsequent heat-treatment. The structural and thermal properties have been systematically studied by thermal analysis, powder XRD, IR spec-troscopy, and XAS. The gallery height of~6.8 $\AA$ upon intercalation of the TCF ion suggests that the $Cr_3O$ plane is parallel to the aluminosilicate layers. Even though the basal spacing of TCF intercalated clay decreases slightly upon heating, the layer structure was retained up to $550^{\circ}C$ as confirmed by XRD and TG/DTA. Ac-cording to the EXAFS spectroscopic analysis, it is identified that the (Cr-Cr) distance of 3.28 $\AA$ between vertex-linked CrO6 octahedra in TCF splits into 2.64 $\AA$, 2.98 $\AA$, and 3.77 $\AA$ due to the face-, edge-, and corner-shared CrO6 octahedra after heating at $400^{\circ}C$, implying that a nano-sized chromium oxide phase was stabilized within the interlayer space of clay.
In vitro 동물세포에서 GGEx18의 ethyl acetate 분획물에 의한 지방산 B-산화효소 유전자 발현의 조절
주병수 ( Byung Soo Joo ),이희영 ( Hee Young Lee ),이혜림 ( Hye Rim Lee ),윤미정 ( Mi Chung Yoon ),서부일 ( Bu Il Seo ),김범회 ( Beom Hoi Kim ),신순식 ( Soon Shik Shin ) 대한본초학회 2012 大韓本草學會誌 Vol.27 No.2
Objectives:This study was undertaken to investigate the effects of the GGEx18 ethyl acetate fraction (EF) on lipid accumulation and gene expression of fatty acid-oxidizing enzymes using 3T3-L1 adipocytes, C2C12 skeletal muscle cells, and NMu2Li liver cells. Methods:PPARa, AMPK and UCPs transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results: 1. Compared with control, EF significantly increased the mRNA expression of VLCAD in 3T3-L1 adipocytes. 2. Compared with control, EF (0.1 ug/ml) significantly inhibited lipid accumulation in 3T3-L1 adipocytes. 3. EF significantly increased the mRNA expression of AMPKa1, AMPKa2 and PPARa in C2C12 skeletal muscle cells compared with control. 4. EF significantly increased the mRNA expression of genes involved in fatty acid b-oxidation, such as thiolase, MCAD, and CPT-1 in C2C12 skeletal muscle cells compared with control. 5. EF significantly increased the mRNA expression of UCP2 involved in energy expenditure in C2C12 skeletal muscle cells compared with control. 6. Compared with control, EF (10 ug/ml) significantly inhibited lipid accumulation in C2C12 skeletal muscle cells. 7. EF (10 ug/ml) significantly increased the mRNA expression of ACOX, HD, VLCAD and MCAD in NMu2Li liver cells compared with control. Conclusions:These results suggest that EF may prevent obesity by increasing the mRNA expression of mitochondrial fatty acid b-oxidizing enzymes in 3T3-L1 adipocytes, by not only regulating the fatty acid oxidation through activation of AMPK and PPARa, but also increasing the UCP2 mRNA expression in C2C12 skeletal muscle cells, and by stimulating the mRNA expression of fatty acid-oxidizing enzymes in NMu2Li liver cells.
In vitro 동물세포에서 GGEx18의 ethyl acetate 분획물에 의한 지방산 β-산화효소 유전자 발현의 조절
신순식,주병수,이희영,이혜림,윤미정,서부일,김범회 대한본초학회 2012 大韓本草學會誌 Vol.27 No.2
Objectives:This study was undertaken to investigate the effects of the GGEx18 ethyl acetate fraction (EF) on lipid accumulation and gene expression of fatty acid-oxidizing enzymes using 3T3-L1 adipocytes, C2C12skeletal muscle cells, and NMu2Li liver cells. Methods:PPARα, AMPK and UCPs transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results: 1. Compared with control, EF significantly increased the mRNA expression of VLCAD in 3T3-L1adipocytes. 2. Compared with control, EF (0.1 ㎍/ml) significantly inhibited lipid accumulation in 3T3-L1 adipocytes. 3. EF significantly increased the mRNA expression of AMPKα1, AMPKα2 and PPARα in C2C12 skeletal muscle cells compared with control. 4. EF significantly increased the mRNA expression of genes involved in fatty acid β-oxidation, such as thiolase, MCAD, and CPT-1 in C2C12 skeletal muscle cells compared with control. 5. EF significantly increased the mRNA expression of UCP2 involved in energy expenditure in C2C12 skeletal muscle cells compared with control. 6. Compared with control, EF (10 ㎍/ml) significantly inhibited lipid accumulation in C2C12 skeletal muscle cells. 7. EF (10 ㎍/ml) significantly increased the mRNA expression of ACOX, HD, VLCAD and MCAD in NMu2Li liver cells compared with control. Conclusions:These results suggest that EF may prevent obesity by increasing the mRNA expression of mitochondrial fatty acid β-oxidizing enzymes in 3T3-L1 adipocytes, by not only regulating the fatty acid oxidation through activation of AMPK and PPARα, but also increasing the UCP2 mRNA expression in C2C12skeletal muscle cells, and by stimulating the mRNA expression of fatty acid-oxidizing enzymes in NMu2Li liver cells.