Derivation of Cinnamon Blocks Leukocyte Attachment by Interacting with Sialosides

PLoS One. 2015 Jun 15;10(6):e0130389. doi: 10.1371/journal.pone.0130389. eCollection 2015.

Abstract

Molecules derived from cinnamon have demonstrated diverse pharmacological activities against infectious pathogens, diabetes and inflammatory diseases. This study aims to evaluate the effect of the cinnamon-derived molecule IND02 on the adhesion of leukocytes to host cells. The anti-inflammatory ability of IND02, a pentameric procyanidin type A polyphenol polymer isolated from cinnamon alcohol extract, was examined. Pretreatment with IND02 significantly reduced the attachment of THP-1 cells or neutrophils to TNF-α-activated HUVECs or E-selectin/ICAM-1, respectively. IND02 also reduced the binding of E-, L- and P-selectins with sialosides. Furthermore, IND02 could agglutinate human red blood cells (RBC), and the agglutination could be disrupted by sialylated glycoprotein. Our findings demonstrate that IND02, a cinnamon-derived compound, can interact with sialosides and block the binding of selectins and leukocytes with sialic acids.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Agglutination / drug effects
  • Anti-Inflammatory Agents / pharmacology
  • Cell Adhesion / drug effects*
  • Cell Line, Tumor
  • Cinnamomum zeylanicum / metabolism*
  • Drugs, Chinese Herbal / pharmacology
  • E-Selectin / metabolism
  • Endothelium, Vascular / metabolism
  • Erythrocyte Aggregation / drug effects*
  • Erythrocytes / drug effects
  • Human Umbilical Vein Endothelial Cells / metabolism*
  • Humans
  • Inflammation / drug therapy
  • Intercellular Adhesion Molecule-1 / metabolism
  • N-Acetylneuraminic Acid / metabolism
  • Neutrophils / metabolism*
  • Orthomyxoviridae / metabolism
  • Proanthocyanidins / pharmacology*
  • Protein Binding / drug effects
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Drugs, Chinese Herbal
  • E-Selectin
  • IND02 polymer
  • Proanthocyanidins
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • N-Acetylneuraminic Acid

Grants and funding

This work was supported by the Center of Infectious Disease and Signaling Research of NCKU and the Ministry of Science and Technology of Taiwan (NSC 102-2321-B-006-006, http://www.most.gov.tw/). Indus Biotech Private Limited provided support in the form of salaries for authors Ekambaranellore Prakash and Mohan Viswaraman, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.