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Ligustilide activates Nrf2/HO‐1 induction, NO synthesis and ameliorates vascular inflammation in HUVECs
Author(s) -
Choi Eun Sik,
Yoon Jung Joo,
Namgung Seung,
Jeong Da Hye,
Kim Hyun Ju,
Lee Yun Jung,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.835.12
Subject(s) - inflammation , phthalide , u937 cell , pharmacology , intracellular , chemistry , tumor necrosis factor alpha , monocyte , umbilical vein , medicine , traditional medicine , immunology , apoptosis , biochemistry , in vitro , organic chemistry
(Z)‐ligustilide is a bioactive phthalide derivative isolated from Cnidii Rhizoma ( Cnidium officinale, rhizome) and Angelicae Gigantis Radix ( Angelica gigas Nakai, root). Vascular endothelium is a central spot in developing cardiovascular diseases and chronic vascular inflammation results in atherosclerosis development. We investigated anti‐inflammatory effects of ligustilide against TNF‐α, and whether ligustilide can activates Nrf2/HO‐1 induction, intracellular NO synthesis in endothelial cells. Ligustilide significantly suppressed adhesion of HL‐60 monocyte to HUVECs via suppressing expression of VCAM‐1, ICAM‐1, and E‐selectin against TNF‐α. Also, ligustilide significantly inhibited ROS production and IκB‐α phosphorylation, and it leaded to suppression of NF‐κB activation. Furthermore, ligustilide up‐regulated induction of HO‐1 via Nrf2 nuclear translocation and synthesis of intracellular NO in HUVECs. Present study demonstrates that ligustilde has vascular protective potential and it might prevents developing cardiovascular complications such as thrombosis or atherosclerosis. Support or Funding Information This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (2008‐0062484).