**5. Conclusions**

In the present study, we found that chronic AA supplementation inhibits the apoptotic and proinflammatory changes and attenuates the exacerbation of cerebral injury and neurological deficits in the diabetic state. These phenomena could be attributed to the antioxidant activity and anti-inflammatory effects of AA. Diabetes repressed the enhancement of SVCT2 expression induced by ischemia-reperfusion in the neurons and capillary endothelial cells, whereas the downregulated expression of SVCT2 was restored to control levels by AA supplementation. Therefore, chronic AA supplementation may enhance and normalize the transport of AA into the CNS and may thus reinforce the antioxidant defense and alleviate oxidative ischemic injury in the brain of diabetic rats.
