Abstract

<h3>Aim</h3> In this study, it was aimed to evaluate effects of dexmedetomidine (DEX) on the damage model induced by hypoxia-ischemia in oxygen and glucose deprivation (OGD) through cell viability (MTT), inflammation (iNOS, eNOS, IL-6, and TGF-b), apoptosis (TUNEL) in the neuroblastoma cell line of mouse origin (NB2a). <h3>Materials and Methods</h3> The effects of DEX on cell viability and toxicity were analyzed with MTT and NTT. Four groups were established for observing the effects of hypoxia-ischemia in the oxygen and glucose deprivation (OGD) model. Control group (C); Cells are incubated with DMEM high glucose medium for 4 hours in normoxic condition. OGY group: Cells are incubated in the oxygen and glucose deprivation (OGD) medium for 4 hours in hypoxic condition which have a gas mixture of 5% CO2, 1% O2 and 92% N2 for 4 hours in hypoxic chamber. DEX+OGD group: Before the OGD procedure, cells are treated with DEX 10 µM for 3 hours. OGD+DEX group: After the OGD procedure, cells were treated with DEX 10 µM for 3 hours. Inflammatory effects were tested by immunohistochemistry and H-scores belonging to antibodies of iNOS, eNOS, and TGF-b were calculated. Apoptotic effects of DEX were tested by the TUNEL method. Data were analyzed one-way ANOVA and Kruskal-Wallis. Data were given mean±SD. p<0.05 is statically significant. <h3>Results</h3> Dexmedetomidine increased the cell viability in those all concentrations (0.1-45 µM) except 60 uM (p<0.01, Figure 1a). H-score value belongs to eNOS antibody decreased significantly with DEX 10 mm in DEX+OGD group and OGD+DEX group compared to OGD group (p<0.001, Figure 1b). H-score value belongs to IL-6 antibody did not show any difference between OGD, DEX+OGD, and OGD+DEX groups (Figure 1d). H-score value belongs to TGF-b antibody significantly decreased with DEX 10 mM in DEX+OGD group and OGD+DEX group compared to OGD group (p<0.0001, Figure 1d). The apoptotic index decreased significantly in the DEX+OGD group and OGD+DEX group compared to Group OGD (p<0.001, Figure 1f) <h3>Conclusions</h3> Dexmedetomidine increased the cell viability in those almost all concentrations (0.1-45 µM) except 60 µM. Either before or after injury treatment with DEX 10 mM decreased apoptosis induced by hypoxia-ischemia in NB2a cells. Treating with DEX 10 mM before OGD injury decreased both iNOS and eNOS antibodies as well. Neuroprotective effects of DEX against OGD injury might be due to antiapoptotic and antioxidative effects.

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