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Chlorella 11-Peptide Inhibits the Production of Macrophage-Induced Adhesion Molecules and Reduces Endothelin-1 Expression and Endothelial Permeability
Department of Pharmacy, Chia-Nan University of Pharmacy & Science, 60 Erh-Te Rd, Sec. 1, Tainan 71710, Taiwan
Department of Pharmacy, Taipei City Hospital, Taipei 10341, Taiwan
Food and Drug Division, Department of Health, Taipei City Government, Taipei 11008, Taiwan
Department of Biochemistry and Chemistry, National Chung Cheng University, 168 University Rd, Chia-Yi 62102, Taiwan
These authors contributed equally to this work.
* Author to whom correspondence should be addressed.
Received: 6 August 2013; in revised form: 13 September 2013 / Accepted: 17 September 2013 / Published: 14 October 2013
Abstract: The inflammation process in large vessels involves the up-regulation of vascular adhesion molecules such as endothelial cell selectin (E-selectin), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) which are also known as the markers of atherosclerosis. We have reported that Chlorella 11-peptide exhibited effective anti-inflammatory effects. This peptide with an amino sequence Val-Glu-Cys-Tyr-Gly-Pro-Asn-Arg-Pro-Gln-Phe was further examined for its potential in preventing atherosclerosis in this study. In particular, the roles of Chlorella 11-peptide in lowering the production of vascular adhesion molecules, monocyte chemoattractant protein (MCP-1) and expression of endothelin-1 (ET-1) from endothelia (SVEC4-10 cells) were studied. The production of E-selectin, ICAM-1, VCAM-1 and MCP-1 in SVEC4-10 cells was measured with ELISA. The mRNA expression of ET-1 was analyzed by RT-PCR and agarose gel. Results showed that Chlorella 11-peptide significantly suppressed the levels of E-selectin, ICAM, VCAM, MCP-1 as well as ET-1 gene expression. The inhibition of ICAM-1 and VCAM-1 production by Chlorella 11-peptide was reversed in the presence of protein kinase A inhibitor (H89) which suggests that the cAMP pathway was involved in the inhibitory cause of the peptide. In addition, this peptide was shown to reduce the extent of increased intercellular permeability induced by combination of 50% of lipopolysaccharide (LPS)-activated RAW 264.7 cells medium and 50% normal SEVC cell culture medium (referred to as 50% RAW-conditioned medium). These data demonstrate that Chlorella 11-peptide is a promising biomolecule in preventing chronic inflammatory-related vascular diseases.
Keywords: endothelium; E-selectin; ICAM-1; VCAM-1; endothelin-1; intercellular permeability
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MDPI and ACS Style
Shih, M.F.; Chen, L.C.; Cherng, J.Y. Chlorella 11-Peptide Inhibits the Production of Macrophage-Induced Adhesion Molecules and Reduces Endothelin-1 Expression and Endothelial Permeability. Mar. Drugs 2013, 11, 3861-3874.
Shih MF, Chen LC, Cherng JY. Chlorella 11-Peptide Inhibits the Production of Macrophage-Induced Adhesion Molecules and Reduces Endothelin-1 Expression and Endothelial Permeability. Marine Drugs. 2013; 11(10):3861-3874.
Shih, Mei F.; Chen, Lih C.; Cherng, Jong Y. 2013. "Chlorella 11-Peptide Inhibits the Production of Macrophage-Induced Adhesion Molecules and Reduces Endothelin-1 Expression and Endothelial Permeability." Mar. Drugs 11, no. 10: 3861-3874.