| Cerebral ischemia is a common disease in old people. Morbidity has been rising progressively along with the increase of the aged people and the coming of senile society. The pathophysiological mechanism of cerebral ischemia disease is related with necrosis and delayed neuronal death after cerebral ischemia reperfusion. Thrombolysis, neuro-protective drugs (including glutamic acid antagonist, Ca2+ pathway blocker etc) and surgical treatment are applied , but their protective effect is unsatisfactory. Though we have already got some research results, there is still lacking of data about its safety. Their application in clinic, therefore, is limited. The new neuro-protective drugs are still in its experimental stage. Traditional Chinese medical theory think that blood stasis due to deficiency of Qi and Toxic materials in blood are the basic mechanism of cerebral I/R. The key factor is that the brain microvascular is impaired by the liver-feng due to toxic materials. Reinforcing genuine Qi, removing stagnaion of blood and getting rid of pathogenic factors are important therapies for cerebral ischemia reperfusion in the aged people.At present, only young animals, instead of old ones, are used to study the mechanism of brain impairment after cerebral I/R. Obviously, it isn't reasonable because of the key factor of aging is ignored. Some efforts have to be made before release of its pathophysiological mechanism and guide to protection of neurocyte and treat disease.1. The nature of neurocyte apoptosis after cerebral ischemia and I/R in the aged rats and the protective effect of Naomaitong This study are reported that ischemia apoptotic cell death of neurons was delayed in the aged SD rats. Age-related changes in the process of neuronal death following acute focal cerebral I/R were studied. The young (4~5 months old) and the aged (20~21 months old) were compared by observation (including oedema by wet-dry/wet, infarct size etc.). This project also employed morphology (including hematoxylin-eosin stain, Nissl stain, electronic microscope etc.), in situ nick-end labeling (TUNEL method) and electrophoresis techniques. The results showed that the infarct size induced by I/R in the brain of aged rats was larger than that of the young, furthermore, the damage area (size and degree) expanded along with the increased extent of ischemia and the prolonged time of reperfusion. Oedema of brain in aged rats induced by I/R demonstrated that no age-related change in the early stage. But the mount of water being taken into brain in the aged rats was significantly greater than in the young with the prolonged time of reperfusion. The degree of brain's damage was also increased with increasing time of reperfusion. The number ofapoptotic cell and apoptotic body changed from time to time. There was a little in the early stage, a lot in the middle stage and a little in the late stage. Necrotis cells rose with time of I/R. This character could be related with aging cells due to the increasing age factor. Naomaitong and Nimodipine could decrease oedema of the brain, diminish the infarct size and improve synhochrome of neuro-damage induced by I/R and reduce histological damage, protect neuron ultrastructure, including to decrease swollen mitochondria and enhance activation of glial cells etc.2. The changes of gene expression of apoptotic cell after I/ R in the aged rats and the protective effect of NaomaitongThis research employed immunohistochemistry, biochemistry and molecular biology techniques to observe dynamically the changes of apoptotic regular gene expression at the different time-point (3h, 6h, 12h, 24h and 72h of MCAO). We measured the brain of 4~5 month-old and 20~21 month-old rats subject to ischemia and reperfusion. Neuro-protective effect of Naomaitong was studied at the same time.2.1. Age-related changes of gene expression of Fas and Fas1 after I/R and neuro-protective effect of NaomaitongThe results showed that gene expression of Fas and Fas1 after I/R happened in all ischemic brain of ra...
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