trimetazidine prevents oxidative changes induced in a rat model of sporadic type of alzheimer's disease.

oxidative stress plays a major role in the pathogenesis of alzheimer's disease (ad) of sporadic origin. the expression of dhcr24 (seladin-1), marker for neuronal oxidative stress and degeneration, has been reported to be altered in the brains of ad patients. in the present study, we investigated the effect of trimetazidine (tmz) on the hippocampal oxidative parameters and the expression of dhcr24 (seladin-1) in an animal model of sporadic ad. male rats were pre-treated with tmz (25 mg/kg) after which injected with intracerebroventricular-streptozotocin (icv-stz)/saline. following 2, 7 and 14 days, animals of different groups were sacrificed with their brain excised to detect the hippocampal lipid peroxidation, superoxide dismutase (sod), catalase activity, dhcr24 (seladin-1) expression and possible histopathological changes. icv-stz administration induced significant oxidative changes in the hippocampus. meanwhile, tmz pre-treatment showed to ameliorate the oxidative stress, which was demonstrated by a significant rise in the hippocampal sod and catalase activity, as well as a significant decrease in the malondialdehyde (mda) level. tmz administration also increased the expression of dhcr24 (seladin-1) gene in the hippocampus. in conclusion, our findings indicated a neuroprotective effect of tmz possibly related to its antioxidant activity resulting in the up-regulation of dhcr24 (seladin-1). such tmz effects may be beneficial in minimizing oxidative stress in sporadic alzheimer's disease and possible prevention of disease progression.