Investigation of the effects of sodium butyrate on SH-SY5Y neurons treated with amyloid beta42 and lipopolysaccharide : A computational and experimental study. / Arabhalvaei, Vida; Rajaei, Seyedeh Niloufar; Alinaghi, Mohammad Mehdi et al.
In: Scientific Reports, Vol. 16, 34113, 23.06.2026.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Investigation of the effects of sodium butyrate on SH-SY5Y neurons treated with amyloid beta42 and lipopolysaccharide
T2 - A computational and experimental study
AU - Arabhalvaei, Vida
AU - Rajaei, Seyedeh Niloufar
AU - Alinaghi, Mohammad Mehdi
AU - Talebi, Mehrshad
AU - Dashti, Fatemeh
AU - Abachi, Seyedeh Fatemeh
AU - Khodayar, Zahra
AU - Jafroodi, Arad Ranji
AU - Jamalaldin, Mohammad
AU - Mehboodi, Mahtab
AU - Maleki, Mohammad Hasan
AU - Rahimi, Atefeh
AU - Baziyar, Payam
N1 - Arabhalvaei, V., Rajaei, S.N., Alinaghi, M.M. et al. Investigation of the effects of sodium butyrate on SH-SY5Y neurons treated with amyloid beta42 and lipopolysaccharide: A computational and experimental study. Sci Rep 16, 34113 (2026). https://doi.org/10.1038/s41598-026-59446-2
PY - 2026/6/23
Y1 - 2026/6/23
N2 - Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid beta42 (Aβ42) aggregation, neuroinflammation, and synaptic dysfunction. This study combines computational and experimental approaches to investigate the neuroprotective effects of sodium butyrate (NaB). Differentiated SH-SY5Y neurons were exposed to lipopolysaccharide (LPS) and Aβ₁₋₄₂ to model AD-like conditions, and the potential protective effects of NaB were evaluated. MD simulations indicated that NaB may be associated with destabilization of organized Aβ₄₂ fibrils. Alterations in RMSD, Rg, and SASA values indicated structural instability of Aβ₄₂ fibrils in the presence of NaB. Treatment with NaB (10 and 50 µM) significantly improved cell viability compared to the LPS + Aβ group (p
AB - Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid beta42 (Aβ42) aggregation, neuroinflammation, and synaptic dysfunction. This study combines computational and experimental approaches to investigate the neuroprotective effects of sodium butyrate (NaB). Differentiated SH-SY5Y neurons were exposed to lipopolysaccharide (LPS) and Aβ₁₋₄₂ to model AD-like conditions, and the potential protective effects of NaB were evaluated. MD simulations indicated that NaB may be associated with destabilization of organized Aβ₄₂ fibrils. Alterations in RMSD, Rg, and SASA values indicated structural instability of Aβ₄₂ fibrils in the presence of NaB. Treatment with NaB (10 and 50 µM) significantly improved cell viability compared to the LPS + Aβ group (p
KW - Болезнь Альцгеймера
KW - NaB
KW - апоптоз
KW - нейровоспаление
KW - Aβ42
KW - молекулярно-динамическое моделирование
KW - Alzheimer’s disease
KW - NaB
KW - Apoptosis
KW - Neuroinflammation
KW - Aβ42
KW - MD simulation
UR - https://www.mendeley.com/catalogue/8d30406e-15ba-3dfc-bd87-54c9e2af44c8/
UR - https://www.scopus.com/pages/publications/105054837181
U2 - 10.1038/s41598-026-59446-2
DO - 10.1038/s41598-026-59446-2
M3 - Article
C2 - 42336952
VL - 16
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 34113
ER -
ID: 84985003