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1.
Acta Pharm ; 67(4): 479-494, 2017 Dec 20.
Article in English | MEDLINE | ID: mdl-29337669

ABSTRACT

In this study, we investigated the gastroprotective effect of an isopropanol extract from the aerial parts of Artemisia princeps (IPAP) and developed a gastroretentive floating tablet of IPAP (IPAP-FR) for maximized local gastroprotective effects. Pre-treatment with IPAP ameliorated the gastric mucosal hemorrhagic lesions in ethanol/HCl- or indomethacin- treated rats. IPAP decreased mucosal hemorrhage of gastric ulcers induced by ethanol or indomethacin plus pyloric ligation in rats. The optimized floating tablet, IPAP-FR, floated on medium surface with more sustained eupatilin release compared to the non-floating control tablet. X-ray photographs in beagle dogs showed that IPAPFR was retained for > 2 h in the stomach. In the ethanol-induced gastric ulcer rat model, the gastric hemorrhagic lesion was improved more substantially with IPAP-FR compared to the non-floating control tablet. Based on these data, our data suggest that IPAP-FR has an improved therapeutic potential for the treatment of gastric ulcer.


Subject(s)
Artemisia/chemistry , Gastric Mucosa/drug effects , Plant Extracts/pharmacology , 2-Propanol , Animals , Anti-Ulcer Agents/pharmacology , Dogs , Ethanol/adverse effects , Flavonoids/pharmacology , Indomethacin/adverse effects , Ligation/adverse effects , Male , Peptic Ulcer Hemorrhage/chemically induced , Peptic Ulcer Hemorrhage/etiology , Peptic Ulcer Hemorrhage/prevention & control , Plant Extracts/administration & dosage , Rats , Rats, Sprague-Dawley , Stomach Ulcer/chemically induced , Stomach Ulcer/complications , Stomach Ulcer/prevention & control , Tablets
2.
Exp Mol Med ; 44(3): 225-35, 2012 Mar 31.
Article in English | MEDLINE | ID: mdl-22192928

ABSTRACT

The integrity of blood vessels controls vascular permeability and extravasation of blood cells, across the endothelium. Thus, the impairment of endothelial integrity leads to hemorrhage, edema, and inflammatory infiltration. However, the molecular mechanism underlying vascular integrity has not been fully understood. Here, we demonstrate an essential role for A-kinase anchoring protein 12 (AKAP12) in the maintenance of endothelial integrity during vascular development. Zebrafish embryos depleted of akap12 (akap12 morphants) exhibited severe hemorrhages. In vivo time-lapse analyses suggested that disorganized interendothelial cell-cell adhesions in akap12 morphants might be the cause of hemorrhage. To clarify the molecular mechanism by which the cell-cell adhesions are impaired, we examined the cell-cell adhesion molecules and their regulators using cultured endothelial cells. The expression of PAK2, an actin cytoskeletal regulator, and AF6, a connector of intercellular adhesion molecules and actin cytoskeleton, was reduced in AKAP12-depleted cells. Depletion of either PAK2 or AF6 phenocopied AKAP12-depleted cells, suggesting the reduction of PAK2 and AF6 results in the loosening of intercellular junctions. Consistent with this, overexpression of PAK2 and AF6 rescued the abnormal hemorrhage in akap12 morphants. We conclude that AKAP12 is essential for integrity of endothelium by maintaining the expression of PAK2 and AF6 during vascular development.


Subject(s)
A Kinase Anchor Proteins/genetics , Blood Vessels/embryology , Embryo, Nonmammalian/blood supply , Gene Expression Regulation, Developmental , Hemorrhage/embryology , Zebrafish/embryology , A Kinase Anchor Proteins/metabolism , Animals , Blood Vessels/abnormalities , Blood Vessels/metabolism , Cell Cycle Proteins/genetics , Cell Cycle Proteins/metabolism , Down-Regulation , Embryo, Nonmammalian/abnormalities , Embryo, Nonmammalian/embryology , Embryo, Nonmammalian/metabolism , Gene Deletion , Hemorrhage/genetics , Hemorrhage/metabolism , Human Umbilical Vein Endothelial Cells , Humans , Intercellular Junctions/genetics , Intercellular Junctions/metabolism , Intercellular Junctions/ultrastructure , Kinesins/genetics , Kinesins/metabolism , Myosins/genetics , Myosins/metabolism , Zebrafish/genetics , p21-Activated Kinases/genetics , p21-Activated Kinases/metabolism
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