Evaluation the protective effects of zinc and selenium co-administration on the oxidative stress in the brain s mitochondria and GPR 39 expression assessed in the rat model of streptozotocin-induced A

Background and Aim : Changes in trace metal concentrations can pathologically lead to neurodegenerative conditions, including zinc (Zn) and selenium (Se) that might be associated with the development of Alzheimer s disease (AD). These metals showed protective effects in the animal model on memory and learning deficits and oxidative stress level via different pathways such as mitochondria.Methods : Male wistar rats were divided in five groups including sham, Alzheimer disease (AD), AD + Zn (10mg/kg, intraperitoneal or i.p, solved in PBS), AD + Se (0.1 mg/kg, i.p, solved in PBS) and AD +Zn/Se co-administration group. Rats pretreated with Zn or/and Se for one week before AD induction via Streptozotocin (STZ, 3 mg/kg/10 μl/rat, intracerebroventricular injection, vehicle: artificial cerebrospinal fluid or aCSF). After two weeks’ recovery period, Spatial memory test via Morris water maze, mitochondria s membrane potential (Δψm) and indexes of mitochondria s oxidative stress including malondialdehyde (MDA) and reactive oxygen species (ROS) as well as glutathione (GSH) and catalase (CAT) plus of GPR39 expression, a zinc receptor, in the brain of rats via Real time PCR were assessed.Results : The indices of spatial memory, all mitochondria s factors (membrane potential and oxidative stress) and GPR39 expression significantly were impaired in AD rats in comparison with the sham group. Co-administration of Zn and Se show more influence on measured factors in current experiment in comparison with the alone injection, but in except of spatial memory test did not significant criteria.Conclusion : Zn/Se co-administration with different pathways such as mitochondria s performance or gene expression may be improved destructed effects of STZ-induced as a model of AD that can overall be present in sign of AD such as memory progression.

کلیدواژه ها:

Alzheimer s disease ، selenium ، zinc ، learning and memory ، Mitochondria s oxidative stress ، GPR39 expression