Evaluation of nickel-induced brain injuries in rats via oxidative stress and apoptosis: attenuating effects of hyperoside

The purpose of this study was to examine whether the administration of nickel (Ni) was associated with cell apoptosis and also to evaluate whether post acute oral exposure to hyperoside would cause histopathologic alterations in rats. Four groups of male Sprague-Dawley rats (n = 7) used in this study were as follows: a control group and groups treated with Ni (as NiCl2, 13 mg/kg), hyperoside (Hyp) (50 mg/kg), and Ni + Hyp. Routine histopathological examination methods such as hematoxylin and eosin (11&E), periodic acid-Schiff (PAS), and Congo red staining for amyloid deposits were applied at the end of the experiment. In addition, biochemical analyses of the rats' brain tissues were carried out. Immunolluorescence (IF) labeling for active caspase 3 was used in the brain sections taken from the Ni-administrated rats to demonstrate the effect of Hyp on the active caspase 3 expression. The rats treated with Ni (13 mg/kg body weight) showed a significant reduction in antioxidant enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase. Furthermore, a significant increase was observed in the levels of thiobarbituric acid reagents. Our data suggested that Ni exposure may contribute to brain damage pathogenesis by mediating neuronal death and increasing the oxidative stress in the rat brain. All these alterations were ameliorated by Hyp administration.