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Keywords:

  • coffee;
  • inflammation;
  • melanoidins;
  • NF-κB;
  • roasting;
  • supercritical CO2 decaffeination

Abstract:  The supercritical CO2-decaffeination process causes unroasted coffee beans to turn brown. Therefore, we suspected that the decaffeinated beans contained melanoidins. Decaffeinated unroasted coffee extract absorbed light at 405 nm with a specific extinction coefficient, Kmix  405  nm, of 0.02. Membrane dialysis (molecular weight cut-off, 12 to 14 kDa) increased the Kmix  405  nm value 15 fold. Gel filtration chromatography showed that the high-MW fraction (MW > 12 kDa) had an elution profile closer to that of melanoidins of medium-roast coffee than to the corresponding fraction of unroasted coffee, indicating the presence of melanoidins in decaffeinated unroasted beans. Using murine myoblast C2C12 cells with a stably transfected nuclear factor-κB (NF-κB) luciferase reporter gene, we found that the high-MW fraction of decaffeinated unroasted beans had an NF-κB inhibitory activity of IC50=  499 μg/mL, more potent than that of regular-roast coffee (IC50= 766 μg/mL). Our results indicate that melanoidins form during the supercritical CO2-decaffeination process and possess biological properties distinct from those formed during the regular roasting process.

Practical Application:  We discovered the roasting effect of decaffeination process, reporting the discovery of melanoidins in green (unroasted) decaf coffee beans. Our results indicated that melanoidins form during the supercritical CO2-decaffeination process and possess biological properties distinct from those formed during the regular roasting process. Our results offer new insights into the formation of bioactive coffee components during coffee decaffeination process.