Selenium reverses zinc-induced differential dendritic remodeling in the dentate gyrus, CA1, and CA3 regions following transient ischemia in rats.

Cerebrovascular disease is a primary global health concern, where ischemia-induced oxidative stress leads to severe neuronal structural damage. The purpose of this study was to evaluate the synergistic potential of prophylactic zinc (Zn) and therapeutic selenium (Se), combined with physical stimulation, in the Morris Water Maze (WMW) to promote neuronal morphological recovery following transient cerebral ischemia. Six experimental groups were: (1) Control, (2) Common Carotid Artery Occlusion (CCAO), (3) Control with Zn (ZnC), (4) Zn + CCAO (5) CCAO + Se, and (6) Zn + CCAO + Se. Neuronal morphology was evaluated 12 days after reperfusion using Golgi-Cox staining to assess the impact of swimming exercise, prophylactic Zn, and therapeutic Se following a 30-minute CCAO protocol. Results showed that swimming training in the MWM did not significantly alter neuronal structure compared with the untreated group. Notably, zinc administration enhanced dendritic arborization in the dentate gyrus (DG) in rats. Furthermore, combined Zn and Se treatment in rats with CCAO improved dendritic arborization and organization in the dentate gyrus (DG) and the CA1 region of the hippocampus. In conclusion, subacute prophylactic Zn administration promotes dendritic remodeling in the DG, while the combination of Zn prophylaxis and Se treatment following CCAO benefits neuronal architecture in both the DG and CA1 regions. Zn and Se supplementation may support post-ischemic neuronal repair, offering a potential adjunct to stroke recovery strategies.