Abstract
We aimed to evaluate the effect of grape seed proanthocyanidins (GSPCs) on neuronal apoptosis, particularly through their roles in maintaining divalent mineral element balance and resisting oxidation in rats with iron overload. A total of 40 Sprague-Dawley rats were randomly divided into control, iron overload, GSPCs, and iron overload + GSPCs groups. The iron, calcium, zinc, magnesium, and copper contents in the brain tissue of the rats were measured using inductively coupled plasma mass spectrometry. Their oxidative stress state was determined using the relevant kit. The number of apoptotic neurons was evaluated using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and synaptosome numbers were determined using the immunohistochemical approach. Fas, Bax, and Bcl-2 gene expressions in the cortex and hippocampus were detected using quantitative real-time polymerase chain reaction. After 7 weeks, compared with the control group, the zinc and magnesium contents; superoxide dismutase, glutathione peroxidase, and catalase activities; and synaptophysin and Bcl-2 gene expressions in the iron overload group were significantly decreased, whereas the iron, calcium contents, and malondialdehyde contents; TUNEL-positive cell numbers; and Fas and Bax gene expressions were significantly increased. There were no significant changes in the copper content. Conversely, the rats exhibited better recovery when GSPCs were used instead of iron alone. In summary, GSPCs protected against iron overload induced neuronal apoptosis in rats by maintaining the divalent mineral element balance, reducing oxidative stress, and regulating apoptotic genes expressions.
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