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Phytoglycoprotein isolated from Dioscorea batatas Decne promotes intestinal epithelial wound healing

Authors
Kim, Ji-YunLee, Young-MinPark, Jong-PilLim, Kye-TaekLee, Sei-Jung
Issue Date
Oct-2020
Publisher
CHINESE JOURNAL NATURAL MEDICINES
Keywords
Cell migration; Dioscorea batatas Decne (DBD) glycoprotein; Intestinal epithelial cells; p38 MAPK; F-actin; Mouse colitis
Citation
CHINESE JOURNAL OF NATURAL MEDICINES, v.18, no.10, pp 738 - 748
Pages
11
Journal Title
CHINESE JOURNAL OF NATURAL MEDICINES
Volume
18
Number
10
Start Page
738
End Page
748
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/63206
DOI
10.1016/S1875-5364(20)60014-0
ISSN
2095-6975
1875-5364
Abstract
Dioscorea batatas Decne (DBD) has been used to heal various illnesses of the kidney and intestine as an herbal medicine in Asia. As a source of therapeutic agents, many glycoproteins have been isolated from mushrooms and plants, but the functional role of glycoprotein in intestinal epithelial wound healing has not been understood yet. In the present study, we investigated the wound healing potentials of the 30 kDa glycoprotein (DBD glycoprotein) isolated from DBD in human intestinal epithelial (INT-407) cells. We found that DBD glycoprotein (100 mu g.mL(-1)) significantly increased the motility of INT-407 cells for 24 h by activating protein kinase C (PKC). DBD glycoprotein stimulated the activation of p38 mitogen-activated protein kinase (MAPK), which is responsible for the phosphorylation of NF-kappa B inhibitor alpha (I kappa B alpha). DBD glycoprotein increased the level of profilin-1 (PFN1), alpha-actinin and F-actin expression via activation of transcription factor, nuclear factor-kappa B (NF-kappa B) during its promotion of cell migration. Experimental mouse colitis was induced by adding dextran sulfate sodium (DSS) to the drinking water at a concentration of 4% (W/V) for 7 days. We figured out that administration of DBD glycoprotein (10 and 20 mg.kg(-1)) lowers the levels of disease activity index and histological inflammation in DSS-treated ICR mice. In this regard, we suggest that DBD glycoprotein has ability to promote the F-actin-related migration signaling events via activation of PKC and NF-kappa B in intestinal epithelial cells and prevent inflammatory bowel disease.
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