title: [Inhibition of arteriosclerotic plaque development by garlic].
abstract: OBJECTIVE
  In an in vitro biosensor model (PCT/EP 97/05212), the interplay between different lipoproteins in arteriosclerotic nanoplaque formation, as well as aqueous garlic extract (0.2-5.0 g/l from LI 111 powder) as a possible candidate drug against arterio/atherosclerosis were tested within the frame of a high throughput screening.
  
  
  METHODS
  The processes described below were studied by ellipsometric techniques quantifying the adsorbed amount (nanoplaque formation) and layer thickness (nanoplaque size). A thorough description of the experimental setup has been given previously.
  
  
  RESULTS
  Proteoheparan sulfate (HS-PG) adsorption to hydrophobic silica was monoexponential and after approximately 30 min constant. The LDL plasma fraction (100 mg/dl) from a healthy probationer showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. Aqueous garlic extract (GE), preferably in a concentration of 1 g/l, applied acutely in the experiment, markedly slowed down this process of ternary aggregational nanoplaque complexation at all Ca2+ concentrations used. In a normal blood Ca2+ concentration of 2.52 mmol/l, the garlic induced reduction of nanoplaque formation and molecular size amounted to 14.8 % and 3.9%, respectively, as compared to the controls. Furthermore, after ternary complex build-up, GE similar to HDL, was able to reduce nanoplaque formation and size. The incubation time for HDL and garlic was only 30 min each in these experiments. Nevertheless, after this short time the deposition of the ternary complex decreased by 6.2% resp. 16.5%, i.e. the complex aggregates were basically resolvable.
  
  
  CONCLUSIONS
  These experiments clearly proved that garlic extract strongly inhibits Ca2+ binding to HS-PG. In consequence, the formation of the ternary HS-PG/LDL/Ca2+ complex, initially responsible for the 'nanoplaque' composition and ultimately for the arteriosclerotic plaque generation, is decisively blunted.
authors.affiliation: Institut für Physiologie, Charité, Campus Benjamin Franklin, Berlin, Deutschland. guenter.siegel@charite.de
authors.forename: Günter
authors.initials: G
authors.lastname: Siegel
authors.forename: Frank
authors.initials: F
authors.lastname: Michel
authors.forename: Michael
authors.initials: M
authors.lastname: Ploch
authors.forename: Miguel
authors.initials: M
authors.lastname: Rodríguez
authors.forename: Martin
authors.initials: M
authors.lastname: Malmsten
mesh_terms: D000327:Adsorption; D001157:Arterial Occlusive Diseases / Q000097:blood* / Q000473:pathology; D001161:Arteriosclerosis / Q000097:blood* / Q000473:pathology; D002114:Calcinosis / Q000097:blood / Q000473:pathology; D002118:Calcium / Q000097:blood; D005737:Garlic; D019812:Heparan Sulfate Proteoglycans / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008954:Models, Biological; D036103:Nanotechnology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology*
chemical_list: D019812:Heparan Sulfate Proteoglycans; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D010936:Plant Extracts; D002118:Calcium