Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-κB activation, and vascular cell adhesion molecule-1 expression in ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-09-30

AUTHORS

Chih-Pei Lin, Yung-Hsiang Chen, Jaw-Wen Chen, Hsin-Bang Leu, Tsan-Zon Liu, Po-Len Liu, Song-Lih Huang

ABSTRACT

Hyperhomocysteinemia is associated with dysfunction and an independent risk factor of cardiovascular diseases. Cholestin (Monascus purpureus-fermented rice), contains a naturally-occurring statin, which has lipid-modulating and anti-inflammatory effects. We investigated the effects of Cholestin extract on the expression of vascular cell adhesion molecule-1 (VCAM-1) by homocysteine (HCY)-treated human aortic endothelial cells (HAECs). Supplement of HAECs with Cholestin extract significantly suppressed cellular binding between the human monocytic cells U937 and HCY-stimulated HAECs. Quantitative PCR and immunoblot analysis showed that Cholestin extract significantly attenuated HCY-induced expression of VCAM-1 mRNA and protein, respectively. Gel shift assays showed that Cholestin treatment reduced HCY-activated transcription factor nuclear factor-κB (NF-κB). Furthermore, Cholestin also attenuated reactive oxygen species (ROS) generation in vitro and in HCY-treated HAECs. Supplement with statins including simvastatin and parastatin gave similar results as compared with Cholestin. In conclusion, Cholestin reduces HCY-stimulated endothelial adhesiveness as well as downregulating intracellular ROS formation, NF-κB activation, and VCAM-1 expression in HAECs, supporting the notion that the natural compound Cholestin may have potential implications in clinical atherosclerosis disease. More... »

PAGES

183-196

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11373-007-9212-0

DOI

http://dx.doi.org/10.1007/s11373-007-9212-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1034348494

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17906965


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