Darbepoetin alpha has neuroprotective effects in the hippocampus against long-term intermittent ethanol administration.

The consumption of ethanol has detrimental effects on several organs, including the brain. One of the most important targets of ethanol toxicity in the brain is the hippocampus. The aim of our study was to investigate the neuroprotective effects of darbepoetin alpha against neuronal damage caused by long-term intermittent ethanol exposure in the hippocampus. Forty male Wistar albino rats were divided into four groups: control (C), ethanol (E), darbepoetin alpha (DA), and ethanol + darbepoetin alpha (E + DA). In this study, oxidative stress and antioxidant markers, S100-β and neuron specific enolase (NSE) were investigated in both brain tissue and serum. Additionally, brain tissues were examined using histopathological methods. S100-β and NSE levels were significantly elevated in the E group compared to the C group in both the brain tissue and serum. Furthermore, catalase (CAT) and glutathione reductase (GR) levels, glutathione peroxidase (GPx) enzyme activities were significantly lower in both brain tissue and serum, while superoxide dismutase (SOD) enzyme activity in brain tissue was significantly reduced, and malondialdehyde (MDA) levels in brain tissue were markedly elevated in the E group. In the E + DA group, S100-β levels in both brain tissue and serum, NSE levels in serum, and MDA levels in brain tissue were significantly lower. Additionally, GPx activity in brain tissue and CAT levels in serum were significantly higher in the E + DA group compared to the E group. Histopathologically, the E group showed moderate neurodegeneration in the dentate gyrus, while the E + DA group exhibited mild neurodegeneration. In conclusion, DA reversed the degenerative effects of long-term intermittent ethanol exposure on the hippocampus by improving oxidative stress parameters and reducing neuronal injury.