Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat

Figure 4

Hematoxylin-eosin staining in slides of the temporoparietal cortex and hippocampus in rats treated with zinc in the presence or absence of L-NAME. Paraffin-embedded tissue sections of 3 μm were stained with hematoxylin and eosin. The Zn96h + CCAO: preventive subacute administration of zinc (2.5 mg/kg each 24 hours for 4 days) and a common carotid-artery occlusion (CCAO) for 10 min. Zn96h + L-NM + CCAO: rats treated with zinc in the presence of an inhibitor of nitric oxide synthase (L-NAME) one hour before a CCAO. CA1 (a–e), CA3 (f–j) regions and dentate gyrus (DG: (k–o)) of hippocampus and LV, layer V of cerebral cortex (p–t). Apoptosis cell (dark arrowhead), necrosis (clear arrowhead), and branched cells (arrow).

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