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Effect of risperidone on proliferation and apoptosis of MC3T3-E1 cells

Lei Zheng1,2, Lixia Yang2, Xin Zhao3

  • 1Department of Mental Health and Psychiatry, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|February 28, 2019
PubMed

Insights

Risperidone use in schizophrenia patients may increase osteoporosis risk by inhibiting preosteoblast cell proliferation and inducing apoptosis. This antipsychotic medication affects key bone metabolism genes, including osteocalcin (BGP).

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Schizophrenia treatment often involves antipsychotics like risperidone.
  • Osteoporosis is a potential side effect linked to risperidone use.
  • The molecular mechanisms underlying this association require elucidation.

Purpose of the Study:

  • To investigate the molecular mechanisms of osteoporosis in schizophrenia patients using risperidone.
  • To assess the effects of risperidone on preosteoblast cell proliferation and apoptosis.

Main Methods:

  • Utilized MC3T3-E1 preosteoblast cell line.
  • Assessed cell viability and apoptosis using cell counting kit-8 and flow cytometry.
  • Quantified mRNA and protein expression of bone metabolism markers (BGP, collagen 1, TNF-α, OPG, RANKL) via qPCR and Western blot.

Main Results:

  • Risperidone significantly inhibited MC3T3-E1 cell proliferation in a dose-dependent manner.
  • Risperidone treatment markedly induced apoptosis in MC3T3-E1 cells.
  • Downregulation of BGP, collagen 1, OPG, and RANKL, with increased TNF-α expression observed.

Conclusions:

  • Risperidone suppresses preosteoblast proliferation and promotes apoptosis.
  • The drug alters the expression of critical genes involved in bone metabolism.
  • Findings suggest a molecular basis for risperidone-associated osteoporosis.

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