Inhibitory functions of cornuside on TGFBIp-mediated septic responses

Transforming growth factor β-induced protein (TGFBIp), as an extracellular matrix protein, is expressed TGF-β in some types of cells. Experimental sepsis is mediated by expressed and released TGFBIp in primary human umbilical vein endothelial cells (HUVECs). Cornuside (CNS) is a bisiridoid glucoside...

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Bibliographic Details
Published inJournal of natural medicines Vol. 76; no. 2; pp. 451 - 461
Main Authors Ryu, Soo Ho, Kim, Chaeyeong, Kim, Nayeon, Lee, Wonhwa, Bae, Jong-Sup
Format Journal Article
LanguageEnglish
Published Singapore Springer Singapore 01.03.2022
Springer Nature B.V
Subjects
Animals
Biomedical and Life Sciences
Biomedicine
Complementary & Alternative Medicine
Endothelial cells
Extracellular matrix
Glucosides - pharmacology
Human Umbilical Vein Endothelial Cells - metabolism
Humans
Immunomodulation
Inflammatory diseases
Lethality
Lipopolysaccharides
Matrix protein
Medicinal Chemistry
Mice
Mice, Inbred C57BL
Original Paper
Pharmacology/Toxicology
Pharmacy
Plant Sciences
Pyrans
Sepsis
Signal transduction
Transforming Growth Factor beta
Transforming growth factor-b
Umbilical vein
Cornuside
Sepsis
HUVEC
TGFBIp
Severe inflammation
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Summary:Transforming growth factor β-induced protein (TGFBIp), as an extracellular matrix protein, is expressed TGF-β in some types of cells. Experimental sepsis is mediated by expressed and released TGFBIp in primary human umbilical vein endothelial cells (HUVECs). Cornuside (CNS) is a bisiridoid glucoside compound found in the fruit of Cornus officinalis SIEB. et ZUCC. Based on the known functions of CNS, such as the immunomodulatory and anti-inflammatory activities, we tested whether TGFBIp-mediated septic responses were suppressed by CNS in human endothelial cells and mice and investigated the underlying anti-septic mechanisms of CNS. Data showed that the secretion of TGFBIp by lipopolysaccharide (LPS) and severe septic responses by TGFBIp were effectively inhibited by CNS. And, TGFBIp-mediated sepsis lethality and pulmonary injury were reduced by CNS. Therefore, the suppression of TGFBIp-mediated septic responses by CNS suggested that CNS may be used as a potential therapeutic agent for several vascular inflammatory diseases, with the inhibition of the TGFBIp signaling pathway as the mechanism of action. Graphical abstract
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ISSN:1340-3443
1861-0293
DOI:10.1007/s11418-021-01601-2