Oral administration of soy-derived genistin suppresses lipopolysaccharide-induced acute liver inflammation but does not induce thymic atrophy in the rat.


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    Views: ()   Date: (2005-11-1)   Pages: ()
  • Author:  Fujio Kayama  

  • Abstract:  Genistein, the principal isoflavone present in soy, has been identified as a protein tyrosine kinase (PTK) inhibitor that has in vitro anti-inflammatory effects. Whether genistein has in vivo anti-inflammatory effects remains unknown yet. Injecting or feeding rats with the unconjugated form of genistein (aglycone) results in decreased thymic weight and lymphocytopenia. However, 95-99% of genistein is present as the conjugated form genistin (genistein glycoside) in soy or soy-derived products. This study was undertaken to reveal whether genistin, as well as genistein, has anti-inflammatory effects in vivo. After oral administration of equimolar genistein (namely 7.4 or 74 micromol/dose) at daily doses of 2.0 or 20 mg/kg, or genistin at daily doses of 3.2 or 32 mg/kg for 3 days to male rats, both aglycone and glycoside suppressed the production of lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 in both from the liver and in the sera. Aglycone induced thymic atrophy while glycoside did not. In vitro preincubation of liver slices from na√Įve rat with genistein aglycone or glycoside suppressed LPS-induced TNF-alpha production in a dose-dependent manner. Taken together, both in vivo and in vitro administration of genistin and genistein suppressed LPS-induced liver pro-inflammatory cytokine production. However, equimolar oral administration of genistin did not induce thymus atrophy. Further investigation in long-term isoflavone intake is required especially among neonates. The results suggest that the safety evaluation of the consumption of isoflavone should be based on isoflavone glycoside but not aglycone.

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