Ipriflavone inhibits phosphoinositide hydrolysis and Ca2+ uptake in the osteoblast-like UMR-106 cells

Maria Angela Sortino*, Grazia Aleppo, Umberto Scapagnini, Pier Luigi Canonico

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


The mechanism of action of ipriflavone, an isoflavone derivative, was studied in the osteoblastic-like UMR-106 cell line. Ipriflavone affected both phosphoinositide hydrolysis and 45Ca2+ uptake. A repeated treatment of UMR-106 cells (once a day, for 3 days) with ipriflavone decreased, in a concentration-dependent manner, [3H]inositol monophosphate accumulation. This effect was also achieved single addition of high concentrations of ipriflavone or 100 nM [Asu1,7]eel-calcitonin, a semi-synthetic analog of eel calcitonin. When repeatedly added to UMR-106 cells, 17β-estradiol produced a marked inhibition of [3H]inositol monophosphate accumulation, an effect which appeared significant only at a concentration of 1 μM and which was accompanied by a reduced incorporation of [3H]inositol into membrane phospholipids. A repeated treatment with ipriflavone reduced 45Ca2+ uptake as well. This effect was observed also after a single addition of [Asu1,7]eel-calcitonin but not following single or repeated treatment with 17β-estradiol. The present data indicate the osteoblast as a direct and specific target for ipriflavone and suggest that this compound may share intracellular transducing mechanisms with other antiosteoporotic hormones such as estrogen and calcitonin.

Original languageEnglish (US)
Pages (from-to)273-277
Number of pages5
JournalEuropean Journal of Pharmacology: Molecular Pharmacology
Issue number3
StatePublished - Jul 1 1992


  • Ca uptake
  • Ipriflavone
  • Phosphoinositides
  • UMR-106 cells

ASJC Scopus subject areas

  • Pharmacology


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