Apoptosis inducing effect of sodium butyrate and cisplatin alone or in combination on SH-SY5Y human neuroblastoma cells

Kaya-Sezginer E., KIRLANGIÇ Ö. F., KARAKAYA C., Ören S., Fatsa T., Özgürtaş T.

Journal of Research in Pharmacy, vol.27, no.1, pp.329-338, 2023 (Scopus) identifier

  • Publication Type: Article / Article
  • Volume: 27 Issue: 1
  • Publication Date: 2023
  • Doi Number: 10.29228/jrp.315
  • Journal Name: Journal of Research in Pharmacy
  • Journal Indexes: Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.329-338
  • Keywords: cisplatin, Histone deacetylase inhibitor, neuroblastoma, SH-SY5Y, sodium butyrate
  • Gazi University Affiliated: Yes


© 2023 Marmara University Press.This study investigated the apoptotic effects of a histone deacetylase (HDAC) inhibitor, sodium butyrate (NaBu) and cisplatin as monotherapy or in combination on SH-SY5Y human neuroblastoma cells. MTT and colony formation assays were performed to investigate the anti-proliferative effects of NaBu in combination with cisplatin. Analysis of SH-SY5Y cell apoptosis was performed by Annexin V-FITC/PI and DAPI staining. The gene and protein expressions were measured by RT-PCR and Western blot. The cytotoxic effect of the combined treatment was higher than single treatments, while the combination of two did not show much higher inhibition of colony formation and induction of apoptosis compared to cisplatin alone. Treatment with cisplatin upregulated the expression of Bax and Bcl-2 and combination treatment enhanced Bax gene expression and Bax/Bcl-2 ratio. NaBu alone and combined with cisplatin enhanced the expression of nuclear factor kappa B (NF-κB) protein, however cisplatin alone significantly decreased NF-κB protein levels. p53 and phosphorylated inhibitor kappa B alpha (p-IκBα) expression did not alter following any of the treatments. The combination of NaBu with cisplatin did not show any additional benefit in SH-SY5Y human neuroblastoma cells compared to cisplatin as a conventional chemotherapeutic agent, probably due to the upregulation of antiapoptotic transcription factor NF-κB.