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Inhibitory Effect of Sulforaphane on Secretory Group IIA Phospholipase A(2)

Authors
Lee, YuriLee, WonhwaKim, JaehongBae, Jong-Sup
Issue Date
2018
Publisher
ASIAN NETWORK SCIENTIFIC INFORMATION-ANSINET
Keywords
Sulforaphane; HUVEC; secretory group IIA phospholipase A2; cecal ligation and puncture; lipopolysaccharide; inflammatory diseases
Citation
INTERNATIONAL JOURNAL OF PHARMACOLOGY, v.14, no.2, pp.187 - 193
Journal Title
INTERNATIONAL JOURNAL OF PHARMACOLOGY
Volume
14
Number
2
Start Page
187
End Page
193
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5212
DOI
10.3923/ijp.2018.187.193
ISSN
1811-7775
Abstract
Background and Objective: The expression of secretory group IIA phospholipase A2 (sPLA2-IIA) has been shown to be elevated in various inflammatory diseases and Lipopolysaccharide (LPS) up-regulates the expression of sPLA2-IIA in Human umbilical vein endothelial cells (HUVECs). Sulforaphane (SFN), a natural isothiocyanate present in cruciferous vegetables such as broccoli and cabbage, is effective in preventing carcinogenesis, diabetes and inflammatory responses. Here, SFN was examined for its effects on the expression and activity of sPLA2-IIA in HUVECs and in mouse models of sepsis. Materials and Methods: After HUVECs were activated with LPS, cells were post-treated with SFN. In vivo, LPS-injected or Ceca I ligation and puncture (CLP) operated mice were administrated SFN. Then, the effects of SFN on the activity and expression of sPLA2-IIA were determined by Enzyme-linked immunosorbent assay (ELISA). The effects of SFN on the activities of cytosolic phospholipase A2 (cPLA2) and Extracellular signal-regulated kinase (ERK)1/2 were monitored. Statistical relevance was determined by one-way analysis of variance (ANOVA). p<0.05 were considered to indicate significance Results: Post-treatment of cells or mice with SFN inhibited LPS- or CLP-ind uced expression and activity of sPLA2-IIA. SFN also suppressed the activation of cPLA2 and ERK1/2 by LPS. Conclusion: It is concluded that, SFN inhibited LPS-mediated expression of sPLA2-IIA by suppression of cPLA2 and ERK1/2.
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