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Peer-reviewedCC BY-NCThe European Chemistry and Biotechnology Journal

In vitro effects of benzydamine on metabolic viability, clonogenic capacity, apoptotic profile, cell-cycle distribution, and inflammation-related gene expression in SH-SY5Y neuroblastoma cells

  1. 1Izmir Kâtip Çelebi University

Abstract

Neuroblastoma (NB) is a pediatric malignancy arising from neural crest–derived sympathetic nervous system cells and is among the most common extracranial solid tumors in children and is characterized by aggressive clinical behavior. Despite advances in multimodal therapies including chemotherapy, radiotherapy, surgery, and immunotherapy, management of high-risk NB remains challenging due to therapy resistance and systemic toxicity in pediatric patients worldwide. Hence, identification of alternative therapeutic agents through drug repurposing has gained increasing attention. Anticancer activity of benzydamine, a nonsteroidal anti-inflammatory drug, was evaluated in SH-SY5Y NB cells. Cell viability was assessed by MTT assay at 24, 48, and 72 h after benzydamine treatment (12.5–100 µM). The compound induced dose- and time-dependent reductions in cell viability with an IC50 of 21.35 µM at 48 h. The colony formation assay showed reduced clonogenic survival following benzydamine treatment, consistent with decreased long-term proliferative capacity. Descriptive flow-cytometric analysis indicated an increased proportion of early apoptotic cells and a decreased viable-cell fraction following treatment at the 48-h IC₅₀ concentration. Similarly, cell-cycle analysis showed a higher proportion of treated cells in the G0/G1 phase than in the untreated control. These findings suggest benzydamine exerts antiproliferative effects via apoptosis induction and cell-cycle disruption. A preliminary qRT-PCR analysis showed modulation of inflammatory cytokine expression at the mRNA level, with notable upregulation of IL6 and IL1β and moderate increases in TNF-α, IFN-γ, IL18, and IL10, indicating a context-dependent inflammatory response following treatment. These preliminary in vitro findings warrant confirmation in independent experiments and additional NB models.

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BibTeX
@article{karahan2026vitro,
  title = {{In vitro effects of benzydamine on metabolic viability, clonogenic capacity, apoptotic profile, cell-cycle distribution, and inflammation-related gene expression in SH-SY5Y neuroblastoma cells}},
  author = {Hatice Ilayhan Karahan and Tulay Kilicaslan Ayna and Cem Sokmen Altintas and Adil Karadag and Asli Eldem},
  journal = {The European Chemistry and Biotechnology Journal},
  year = {2026},
  month = oct,
  doi = {10.62063/ecb-92},
  url = {https://doi.org/10.62063/ecb-92},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - In vitro effects of benzydamine on metabolic viability, clonogenic capacity, apoptotic profile, cell-cycle distribution, and inflammation-related gene expression in SH-SY5Y neuroblastoma cells
AU  - Hatice Ilayhan Karahan
AU  - Tulay Kilicaslan Ayna
AU  - Cem Sokmen Altintas
AU  - Adil Karadag
AU  - Asli Eldem
PY  - 2026
DA  - 2026/10/29
JO  - The European Chemistry and Biotechnology Journal
DO  - 10.62063/ecb-92
UR  - https://doi.org/10.62063/ecb-92
AB  - Neuroblastoma (NB) is a pediatric malignancy arising from neural crest–derived sympathetic nervous system cells and is among the most common extracranial solid tumors in children and is characterized by aggressive clinical behavior. Despite advances in multimodal therapies including chemotherapy, radiotherapy, surgery, and immunotherapy, management of high-risk NB remains challenging due to therapy resistance and systemic toxicity in pediatric patients worldwide. Hence, identification of alternative therapeutic agents through drug repurposing has gained increasing attention. Anticancer activity of benzydamine, a nonsteroidal anti-inflammatory drug, was evaluated in SH-SY5Y NB cells. Cell viability was assessed by MTT assay at 24, 48, and 72 h after benzydamine treatment (12.5–100 µM). The compound induced dose- and time-dependent reductions in cell viability with an IC50 of 21.35 µM at 48 h. The colony formation assay showed reduced clonogenic survival following benzydamine treatment, consistent with decreased long-term proliferative capacity. Descriptive flow-cytometric analysis indicated an increased proportion of early apoptotic cells and a decreased viable-cell fraction following treatment at the 48-h IC₅₀ concentration. Similarly, cell-cycle analysis showed a higher proportion of treated cells in the G0/G1 phase than in the untreated control. These findings suggest benzydamine exerts antiproliferative effects via apoptosis induction and cell-cycle disruption. A preliminary qRT-PCR analysis showed modulation of inflammatory cytokine expression at the mRNA level, with notable upregulation of IL6 and IL1β and moderate increases in TNF-α, IFN-γ, IL18, and IL10, indicating a context-dependent inflammatory response following treatment. These preliminary in vitro findings warrant confirmation in independent experiments and additional NB models.
SN  - 3023-5839
ER  -