Scopolamine-induced brain injury
A recent study by Chen et al154 reported the therapeutic effects of LBPs on learning and memory and neurogenesis in scopolamine (SCO)-treated adult male Sprague–Dawley rats. SCO was used to induce learning and memory deficits. LBPs were administered 0.2 mg/kg or 1 mg/kg body weight per day via gastric perfusion for 14 days before the onset of subcutaneous SCO treatment for a further 4 weeks. LBPs used were extracted with boiling water, followed by precipitation with ethanol, protein hydrolysis, dialysis, and fractionation with a diethylaminoethanol-Sepharose CL-6B column. An osmotic pump containing SCO solution at 440 mg/mL was subcutaneously embedded in the abdominal wall of rats and SCO release at a rate of 0.25 µL/h was maintained for 28 days and administration of LBPs was continued as before, throughout SCO treatment. LBPs at both doses almost restored the memory and learning abilities in SCO-treated rats.154 LBPs prevented SCO-induced reduction in neuronal proliferation and enhanced neuroblast differentiation in the hippocampal dentate gyrus of rats.
LBP treatment also protected the dendrites from damage by SCO. LBPs dose-dependently decreased the SCO-induced oxidative stress in hippocampus and reversed the increased ratio of Bax/Bcl-2 induced by SCO treatment.154 LBPs significantly increased hippocampal SOD and GPx activity and reduced MDA level in SCO-treated rats. However, LBPs did not affect the SCO-induced elevation of hippocampal acetylcholinesterase activity and decrease of brain-derived neurotrophic factor level.154 These results suggest that LBPs prevent SCO-induced cognitive and memory impairments and reductions in hippocampal cell proliferation and neuroblast differentiation. Anti-oxidation and anti-apoptosis are the two major mechanisms for the neuroprotective effects of LBPs in SCO-treated rats (Figure 12).