• B Cebeci, E E Yalinbas, R Akcilar, and H Metineren.
• Bratisl Med J. 2020 Jan 1; 121 (11): 789-795.

AimsHypoxic ischemic encephalopathy is one of the main causes of neonatal deaths. The objective of this study was to evaluate the neuroprotective effect of antioxidant and anti-inflammatory properties of sodium hydrosulfide (NaHS) in neonatal rats with hypoxic ischemic encephalopathy, as well as its effect on neuronal apoptosis through histopathological and biochemical tests.MethodsForty-seven-day‑old rats with induced hypoxia‑ischemia (HI) were randomly separated into four groups. Half an hour after the induction of hypoxic-ischemia, serum physiological (SF), 50 µmol/kg NaHS, or 100 µmol/kg NaHS were intraperitoneally given to the rats.ResultsApoptotic cells in the brain tissue of rats in HI + NaHS 50 μmol/kg, and HI + NaHS 100 μmol/kg groups decreased compared to HI group (p = 0.00). While HI + NaHS 50 μmol/kg and HI + NaHS 100 μmol/kg groups yielded no difference in TNF-α, IL-6, and iNOS levels as compared to the HI group, an increase in NGF was detected in the 50 µmol/kg and 100 µmol/kg NaHS groups (p = 0.34, p = 0.24, p = 0.26, p = 0.026, p = 0.017). When TOS, TAS and OSI levels were compared, an increase in TAS and OSI and a decrease in TOS were observed in the treatment groups as compared to HI group.ConclusionsNaHS given to hypoxic-ischemic encephalopathy model significantly decreased apoptosis in neurons and had a neuroprotective efficacy with an increase in NGF levels (Tab. 1, Fig. 3, Ref. 25).

16 keywords...

hide…