@misc{Ziąbska-Pacześ_Karolina_Wpływ_2026,
 author={Ziąbska-Pacześ, Karolina},
 editor={Nałęcz, Małagorzata (Promotor)},
 copyright={Creative Commons Attribution BY 4.0 license},
 address={Warszawa},
 howpublished={online},
 year={2026},
 school={Mossakowski Medical Research Institute Polish Academy of Sciences},
 language={pol},
 abstract={Perinatal hypoxic-ischemic brain damage can lead to long-term neurological disorders. Despite increasing knowledge of the pathomechanisms of brain damage after asphyxia, effective therapy has yet to be developed. Recent studies have shown that histone deacetylase inhibitors can have a protective effect on the nervous system. The complement system plays a crucial role as a mediator of inflammation. In the acute phase of ischemia, complement activation occurs, leading to the elimination of synaptic connections by pro- inflammatory microglia. For this reason, we conducted an investigation into complement and microglia activation and changes in the structure of synapses and neurons in an in vivo and in vitro animal model of perinatal asphyxia, as well as the effect of the histone deacetylase inhibitor – sodium butyrate – on these processes. Additionally, we investigated the effect of sodium butyrate on locomotor function in animals after hypoxia-ischemia. We also determined the effect of sodium butyrate on selected signaling pathways involved in microglial activation using the BV2 cell line. We demonstrated the anti-inflammatory effects of sodium butyrate by inhibiting complement activation after perinatal asphyxia. We also demonstrated a reduction in the expression of pro- inflammatory markers and an increase in the expression of anti-inflammatory markers in BV2 cells. One of the molecular mechanisms of the sodium butyrate’s action may be activation of the PI3K/AKT pathway. Furthermore, we demonstrated a neuroprotective effect of butyrate by reducing the elimination of synaptic proteins in an in vivo model and improving the degree of branching of neuronal processes in an in vitro model. However, we did not observe differences in locomotor function between the experimental groups analysed. The results obtained indicate that sodium butyrate is a substance that could contribute to the development of a new therapeutic strategy to reduce brain damage caused by perinatal asphyxia.},
 type={Text},
 title={Wpływ inhibitora deacetylaz histonów-maślanu sodu- na aktywność układu dopełniacza w modelu okołoporodowego hipoksyjno-ischemicznego uszkodzenia mózgu u szczura},
 URL={http://rcin.org.pl/imdik/Content/260809/Ziabska-Paczes_Karolina_l.pdf},
 keywords={Complement system, Hypoxia-ischemia, Sodium-butyrate},
}