Cerebrolysin attenuates ethanol-induced spatial memory impairments through inhibition of hippocampal oxidative stress and apoptotic cell death in rats.

Abstract

The present study investigates the potential neuroprotective effect of cerebrolysin (CBL), a combination of neurotrophic factors, on the cognitive and biochemical alterations induced by chronic ethanol administration in rats. The animals were divided into five groups as follows: control; ethanol (4g/kg, for 30 days) plus normal saline (Ethanol+NS); ethanol plus CBL 1mL/kg (Ethanol+CBL 1), ethanol plus CBL 2.5mL/kg (Ethanol+CBL 2.5); and ethanol plus CBL 5mL/kg (Ethanol+CBL 5). The Morris water maze (MWM) test was performed to assess cognitive impairment. The status of the lipid peroxidation marker MDA, antioxidant capacity, as well as alterations of the apoptotic factors such as Bcl-2, BAX, and cleaved caspase-9 and -3, were evaluated in the hippocampus. The results showed that CBL treatment not only normalized the increased MDA levels in the alcoholic rats and enhanced antioxidant defense, but also reduced the Bax/Bcl-2 ratio and cleaved caspase-9 and -3 in the hippocampus. These results were parallel with improvement in spatial memory performance in the MWM test. The findings of the present study provide evidence for the promising therapeutic effect of CBL in chronic ethanol consumption through counteracting oxidative stress and apoptosis markers.