Isoferulic acid, a new anti-glycation agent, inhibits fructose- and glucose-mediated protein glycation in vitro

Molecules. 2013 May 30;18(6):6439-54. doi: 10.3390/molecules18066439.

Abstract

The inhibitory activity of isoferulic acid (IFA) on fructose- and glucose-mediated protein glycation and oxidation of bovine serum albumin (BSA) was investigated. Our data showed that IFA (1.25-5 mM) inhibited the formation of fluorescent advanced glycation end products (AGEs) and non-fluorescent AGE [Nε-(carboxymethyl) lysine: CML], as well as the level of fructosamine. IFA also prevented protein oxidation of BSA indicated by decreasing protein carbonyl formation and protein thiol modification. Furthermore, IFA suppressed the formation of β-cross amyloid structures of BSA. Therefore, IFA might be a new promising anti-glycation agent for the prevention of diabetic complications via inhibition of AGEs formation and oxidation-dependent protein damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cinnamates / chemistry
  • Cinnamates / pharmacology*
  • Fructose / chemistry*
  • Glucose / chemistry*
  • Glycation End Products, Advanced / chemistry
  • Glycation End Products, Advanced / metabolism
  • Glycosylation / drug effects
  • Proteins / chemistry*
  • Proteins / metabolism*
  • Serum Albumin, Bovine / chemistry
  • Serum Albumin, Bovine / metabolism

Substances

  • Cinnamates
  • Glycation End Products, Advanced
  • Proteins
  • Serum Albumin, Bovine
  • Fructose
  • Glucose
  • isoferulic acid