| Keywords |
Intracerebral hemorrhage ; Swimming ; Nitric oxide synthase ; Hippocampus |
| Abstract |
Intracerebral hemorrhage is one of the most devastating types of stroke. This disease is known to cause severe neurological damage and also has a very high mortality rate. Nitric oxide (NO) is synthetized from L-arginine by nitric oxide sy nthase (NOS). NO play many physiological functions, however excessive NO production induces neuronal cell death. There are three distinct isoforms of NOS: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). In the present study, we investigated the effect of swimming on nitric oxide synthase expression in the hippocampal CA1 region following intracerebral hemorrhage using rats. Intracerebral hemorrhage was induced by injection of collagenase into the hippocampal CA1 region using a stereotaxic instrument. The rats were divided into 3 groups: the sham-operation group, the hemorrhage-induction group, and the hemorrhage-induction and swimming group. The animals in the swimming group performed swimming for 30 min once a day during 14 consecutive days. For this experiment, Nissl staining, nNOS immunohistochemistry, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry were performed. In the present results, induction of intracerebral hemorrhage caused neuronal cell death in the hippocampal CA1 region, while swimming decreased hemorrhage-induced neuronal death (p<0.05). The numbers of nNOS-positive cells and NADPH-d-positive cells in the hippocampal CA1 region were significantly increased following induction of intracerebral hemorrhage (p<0.05). Swimming suppressed the numbers of hemorrhage-induced nNOS-positive cells and NADPH-d-positive cells in the hippocampal CA1 region (p<0.05). Here in this study, we have shown that swimming inhibited intracerebral hemorrhage-induced NOS expression and thus exerted neuroprotective effect against intracerebral hemorrhage. |