Postischemic Housing Environment on Cerebral Metabolism and Neuron Apoptosis after Focal Cerebral Ischemia in Rats.

The purpose of this study was to evaluate the roles of different housing environments in neurological function, cerebral metabolism, cerebral infarction and neuron apoptosis after focal cerebral ischemia. Twenty-eight Sprague-Dawley rats were divided into control group (CG) and cerebral ischemia group, and the latter was further divided into subgroups of different housing conditions: standard environment (SE) subgroup, individual living environment (IE) subgroup, and enriched environment (EE) subgroup. Focal cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO). Beam walking test was used to quantify the changes of overall motor function. Cerebral infarction and cerebral metabolism were studied by in vivo magnetic resonance imaging and 1H-magnetic resonance spectra, respectively. Neuron necrosis and apoptosis were detected by hematoxylin-eosin and TUNEL staining methods, respectively. The results showed that performance on the beam-walk test was improved in EE subgroup when compared to SE subgroup and IE subgroup. Cerebral infarct volume in IE subgroup was significantly larger than that in SE subgroup (P<0.05) and EE subgroup (P<0.05) on day 14 after MCAO. NAA/Cr and Cho/Cr ratios were lower in MCAO groups under different housing conditions as compared to those in CG (P<0.05). NAA/Cr ratio was lower in IE subgroup (P<0.05) and higher in EE subgroup (P<0.05) than that in SE subgroup. NAA/ Cr ratio in EE was significantly higher than that in IE subgroup (P<0.05). Cho/Cr ratio was decreased in MCAO groups as compared to that in CG (P<0.05). A significant decrease in normal neurons in cerebral cortex was observed in MCAO groups as compared to CG (P<0.05). The amount of normal neurons was less in IE subgroup (P<0.05), and more in EE subgroup (P<0.05) than that in SE subgroup after MCAO. The amount of normal neurons in EE subgroup was significantly more than that in IE subgroup after MCAO (P<0.05). The ratio of TUNEL-positive neurons in EE was significantly lower than that in SE subgroup (P<0.05) and IE subgroup (P<0.05). Correlation analysis showed that the beam walking test was negatively correlated with NAA/Cr ratio (P<0.05). Cerebral infarct volume was negatively correlated with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.01). The amount of normal cortical neurons was positively correlated with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.05). The TUNEL-positive neurons showed a negative correlation with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.01). This study goes further to show that EE may improve neurological functional deficit and cerebral metabolism, decrease cerebral infarct volume, neuron necrosis and apoptosis, while IE may aggravate brain damage after MCAO.