Akademik Veri Yönetim Sistemi
NEUROENDOCRINOLOGY, cilt.113, sa.9, ss.924-929, 2023 (SCI-Expanded)
Introduction: The aim of this study was to investigate whether Cortexin (R), a brain peptide containing agent, has any mitigating effect on high glucose-induced neuropathy using primary cultured rat sensory neurons.Materials and Methods: Dorsal root ganglia (DRG) were excised from decapitated adult rats. Individual neurons were isolated following enzymatic and mechanical procedures. Cells were seeded on E-Plate (R) with gold microelectrodes, and maintained in conventional culture media in a CO2 incubator at 37 oC. After allowing for 24 hours for cell adhesion and recovery from acute enzymatic trauma, neurons were exposed to high glucose (HpG) in the absence and presence of different concentrations of Cortexin (R) (2- 40 mu g/ml). Neuroprotective effects were followed with the Real-Time Cell Analyzer (R) by utilizing measurement of Cell Index, a parameter representing cell viability, cell attachment and neurite outgrowth.Results: Exposure of DRG's to HpG (50 mM) caused a rapid and sustained decrease in the mean area under curve (AUC, values derived from time vs. Cell Index curve) compared to the mean AUC values in NG wells. Co-treatment with Cortexin (R) attenuated this HpG-induced effect, in a concentration-dependent manner (NG: 1.00 +/- 0.00 vs HG: 0.18 +/- 0.02, P<0.05; and HpG + Cortexin (R) (40 mu g/ml): 0.66 +/- 0.17, P=0.002 vs HpG). In normoglycemic conditions, Cortexin (R) treatment led to a concentration-dependent increase in the mean AUC values.Conclusions: Data from this in vitro study suggests that Cortexin (R) has potential neuroprotective effects against chronic hyperglycemic insult in rat sensory neurons. Our results warrants further in vivo studies and may have clinical implications for diabetes-associated peripheral neuropathy.