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Effects of newly synthesized benzimidazole derivatives on gastric H^+/K^+$ ATPase
Cheon, Hyae-Gyeong,Yum, Eul-Kgun,Kim, Sung-Soo The Pharmaceutical Society of Korea 1996 Archives of Pharmacal Research Vol.19 No.2
The effects of various synthetic benzimidazole derivatives on gastric H^+/K^+$ATPase activity in vitro were examined. The results showed that the effects of substituents on the benzimidazole ring were not significant. However, replacement of sulfoxide connecting two ring systems to sulfide resulted in a completely inactive compound in vitro, suggesting the essential role of sulfoxide group in the inhibition. In addition, compounds with 5 or 6-membered oxacyclic substituents attached to the pyridine ring displayed the most effective inhibitory activity. Among these derivatives, AU-47 was the most potent, and detailed mechanistic studies with the compound were carried out. AU-47 inhibited gastricH^+/K^+$ATPase in a concentration and time dependent manner with 50% inhibition at $6\muM$. The presence of sulfhydryl reducing agents or substrate analogue protected H^+/K^+$ATPase from the inactivation. The inhibition by AU-47 was potentiated by acid pretreatment of the compound, suggesting the structural conversion of AU-47 into a more active intermediate which was favored in acidic condition. Consistent with in vitro results, AU-47 inhibited in vivo gastric acid secretion. The results suggest that AU47 is a relevant candidate for the development of new antiulcer agent.
Anti-Ulcer Activity of Newly Synthesized Acylquinoline Derivatives
Cheon, Hyae-Gyeong,Kim, Hyun-Jung,Mo, Hye-Kyoung,Shin, En-Joo,Lee, Yeon-Hee The Pharmaceutical Society of Korea 1999 Archives of Pharmacal Research Vol.22 No.2
Anti-ulcer activity of newly synthesized acylquinoline derivatives was investigated. For the in vitro screening, the effects of compounds on gastric $H^{+}/K^{+}$ ATPase isolated from hog and rabbit were examined. Among them, AU-090, AU-091, AU-254, AU-413 and AU-466 exhibited good in vitro activity on both enzymes. To correlate the in vitro activity with in vivo action, the effects of the compounds on the basal gastric acid secretion were studied. Some derivatives showed considerable anti-secretory activities, and AU-413 was selected for further studies. AU-413 protected gastric damage induced by either ethanol or NaOH dose dependently when given orally. $ED_{50}$ values of 12 mg/kg, p.o. (ethanol) and 41 mg/kg, p.o. (NaOH) were obtained. In addition, histamine-stimulated gastric secretion was reduced upon AU-413 administration. Taken together, newly synthesized acylquinoline derivatives, especially AU-413, is worthy of further investigation to be developed as an anti-ulcer agent.
Cheon, Hyae Gyeong,Cho, Young Sik BioMed Central 2014 JOURNAL OF BIOMEDICAL SCIENCE -BASEL- Vol.21 No.1
<P><B>Background</B></P><P>Excessive saturated fatty acids have been considered to be one of major contributing factors for the dysfunction of skeletal muscle cells as well as pancreatic beta cells, leading to the pathogenesis of type 2 diabetes.</P><P><B>Results</B></P><P>PA induced cell death in a dose dependent manner up to 1.5 mM, but AA protected substantially lipotoxicity caused by PA at even low concentration of 62 μM, at which monounsaturated fatty acids including palmitoleic acid (POA) and oleic acid (OA) did not protect as much as AA did. Induction of cell death by PA was resulted from mitochondrial membrane potential loss, and AA effectively blocked the progression of apoptosis. Furthermore, AA rescued significantly PA-impaired glucose uptake and -signal transduction of Akt in response to insulin.</P><P>Based on the observations that polyunsaturated AA generated competently cellular droplets at low concentration within the cytosol of myotubes compared with other monounsaturated fatty acids, and AA-driven lipid droplets were also enhanced in the presence of PA, we hypothesized that incorporation of harmful PA into inert triglyceride (TG) may be responsible for the protective effects of AA against PA-induced lipotoxicity. To address this assumption, C2C12 myotubes were incubated with fluorescent probed-PA analogue 4, 4-difluoro-5, 7-dimethyl-4-boro-3a,4a-diaza-<I>s</I>-indacene-3-hexadecanoic acid (BODIPY FL C16) in the presence of AA and their subsequent lipid profiles were analyzed. The analyses of lipids on thin layer chromatograpy (TLC) showed that fluorescent PA analogue was rapidly channeled into AA-driven TG droplets.</P><P><B>Conclusion</B></P><P>Taken together, it is proposed that AA diverts PA into inert TG, therefore reducing the availability of harmful PA into intracellular target molecules.</P>
Effect of Heparin on the High Affinity KGF and aFGF Binding to the Chimeric KGFR - HFc
Cheon, Hyae Gyeong 생화학분자생물학회 1981 BMB Reports Vol.29 No.3
To investigate the role of heparin in keratinocyte growth factor (KGF) and acidic fibroblast growth factor (aFGF) high affinity binding to the KGF receptor (KGFR), a cell free system was established which utilized a secreted chimeric molecule between the KGFR extracellular domain and the immunoglobulin heavy chain Fc domain (KGFR-HFc). KGFR-HFc was purified from NIH 3T3 cells and demonstrated the binding of [³H]-heparin as well as heparin Sepharose, Scatchard analysis showed that the dissociation constant for heparin binding to KGFR-HFc was 140 nM. High affinity KGF and aFGF binding to KGFR-HFc remained unchanged after treatment with 0.6 M NaCI, which is the concentration sufficient to release any bound heparin to the KGFR-HFc. These results strongly suggest that although the KGFR interacts with heparin, the presence of heparin is not absolutely required for high affinity binding of either KGF or aFGF to the KGFR.
Effect of Heparin on the High Affinity KGF and aFGF Binding to the Chimeric KGFR-HFc
Cheon, Hyae-Gyeong Korean Society for Biochemistry and Molecular Biol 1996 Journal of biochemistry and molecular biology Vol.29 No.3
To investigate the role of heparin in keratinocyte growth factor (KGF) and acidic fibroblast growth factor (aFGF) high affinity binding to the KGF receptor (KGFR), a cell free system was established which utilized a secreted chimeric molecule between the KGFR extracellular domain and the immunoglobulin heavy chain Fc domain (KGFR-HFc). KGFR-HFc was purified from NIH 3T3 cells and demonstrated the binding of $[^3H]-heparin$ as well as heparin Sepharose. Scatchard analysis showed that the dissociation constant for heparin binding to KGFR-HFc was 140 nM. High affinity KGF and aFGF binding to KGFR-HFc remained unchanged after treatment with 0.6 M NaCl, which is the concentration sufficient to release any bound heparin to the KGFR-HFc. These results strongly suggest that although the KGFR interacts with heparin, the presence of heparin is not absolutely required for high affinity binding of either KGF or aFGF to the KGFR.