Pretreatment with a histone deacetylase inhibitor, sodium butyrate, potentiates the sustained expression of myelin-associated and neurotrophic genes in cultured Schwann cells.

Schwann cells have therapeutic potential for central nervous system repair, but their limited posttransplant survival remains a major challenge. Because histone deacetylase inhibitors (HDACIs) can enhance genes involved in myelination potential and neurotrophic support, this study investigated whether sodium butyrate (NaB), an HDACI, promotes the expression and sustained regulation of myelin‑associated and neurotrophic genes in cultured Schwann cells. Cultured Schwann cells were treated with 1 or 10 mM NaB for either 48 h (prolonged treatment) or 24 h followed by reagent washout (transient treatment). Expression of myelin-associated genes, neurotrophic factors, and apoptosis marker were quantified using quantitative reverse transcription PCR. Cell viability was assessed via Cell Counting Kit-8 assay. Prolonged treatment with NaB increased the expression of myelin-associated genes ( Mbp and Mpz ) and neurotrophic genes ( Igf-1 and Gdnf ). Furthermore, transient NaB treatment increased these gene expressions for up to 24 h after reagent washout and attenuated NaB‑induced apoptosis. Specifically, transient treatment with a high dose of NaB strongly sustained the enhanced expression of the myelin marker, Mpz . Transient pre‑treatment with NaB enhanced and sustained the expression of certain key myelin‑associated and neurotrophic genes in Schwann cells while reducing cytotoxic effects. These findings suggest a potential strategy to improve certain Schwann cell functions and support further investigation of HDACI‑based approaches in regenerative therapy.