| Objective: Vascular Dementia is one of the main types of geriatric dementia, and it is caused by a series of cerebral vessels factor, such as ischemic, sanguinis profluvium and hypoxia cerebrovascular disease. Vascular Dementia is a kind of dementia syndrome with recognition functional disturbance. It not only takes long-term anguish to the patient, but also poses heavy burden on the family and society. So the studies of pathogenesis for Vascular Dementia have very important social value and practical importance. Hydrogen sulfide (H2S) is a kind of gas with brom-egg taste. It has toxic action, but it also participate many physiological and path process in organism, so it is regard as the third kind of gas signaling molecule after nitric oxide and carbon monoxide. Hydrogen sulfide can play an important role in nervous system, and it also can be an endogenic anti-oxidant to remove active oxygen for example hydroxyls radical and protect the nerve cells. The research observed the capability of learning and memory, contents of hydrogen sulfide in blood serum and nerve cells apoptosis in CA1 region of hippocampus in Vascular Dementia rats of cerebral ischemia reperfusion different time, investigated the pathogenesis of Vascular Dementia, knowed the effect of H2S as a new gas signaling molecule and provided theory evidence for Vascular Dementia's prevention and cure.Methods: 64 healthy male Wister rats were randomly divided into 8 groups: Normal group, Sham-operated group and IR groups, IR group were divided into IR 2h group, IR 8h group, IR 24h group, IR 72h group, IR 168h group and IR 720h group (n=8 each). Using the method of 4-VO, the animal Vascular Dementia models were established. The capability of learning and memory were tested by Morris water maze, cerebrum morphology were observed by light microscope, the expression of Bcl-2 and Bax were detected by immunohistochemistry staining method, and the average optical density values of masc. target in CA1 region of hippocampus were measured by Motic6.0 medical image analysis system. The apoptosis rates of nerve cells in hippocampus were detected by flow cytometry, and the contents of hydrogen sulfide in blood serum were detected by methylene blue chromatometry. All the experimental data used SPSS13.0 software for statistics analysis.Results: 1. Behavior science: All rats shortened their escape latency following with the increasing of training time, and statistics difference began to appear in sequenti luce of training. Escape latency was significantly longer in the IR 720h group compared to Normal group and Sham-operated group (P<0.01), escape latency was not statistically significant in Normal group compared to Sham-operated group (P>0.05). 2. Morphology: Nerve cells in CA1 region of hippocampus of Sham-operated group were integrity and normal with abundant endochylema, cell nucleus presented round or ellipse, no cell nucleus pyknosis or dissolving emerged, chromatin distributed uniformity, and interstitial substance had no dropsy. Neuronal degeneration phenomenon could be seen in the model group. Nerve cells volume shrinked, nucleus and endochylema had no clear margin and nerve cells emerged karyopycnosis. The amounts of degeneration nerve cells were more following with the extending time of ischemic reperfusion. 3. Expression of apoptosis protein: The average optical density values of both the anti-apoptotic protein Bcl-2 and the pro-apoptotic protein Bax were up-regulated, during reperfusion after 2h of ischemia, the expression of Bcl-2 was induced with peak expression at 8h, and then decreased, but the expression of Bcl-2 was higher in the reperfusion after 24h of ischemia compared to Sham-operated group (P<0.05). The average optical density values of Bax increased with time after reperfusion with peak expression at 72~168h (P<0.05). The ratios of Bcl-2/Bax decreased following with the extending time of ischemic reperfusion. 4. The apoptosis rates of nerve cells in hippocampus: The apoptosis rates of nerve cells in hippocampus were up-regulated in the model groups compared to Sham-operated group (P<0.01), and the apoptosis rates of nerve cells in hippocampus increased following with the extending time of ischemic reperfusion and presented an increasing tendency of logarithmic curve. 5. Contents of hydrogen sulfide in blood serum: The contents of hydrogen sulfide in blood serum of the model groups reduced compared to Normal group and Sham-operated group (P<0.01), and decreased straightly following with the extending time of ischemic reperfusion. 6. The correlation analysis for contents of serum hydrogen sulfide and apoptosis rates of hippocampus nerve cells: The apoptosis rates of hippocampus nerve cells heightened following with the decreasing of the contents of serum hydrogen sulfide, they presented linearity correlation relation and they might be the cues of endogenous hydrogen sulfide protecting nerve cells from apoptosis.Conclusion: Cerebral ischemia reperfusion injury resulted in the impairment of learning and memory, apoptosis of nerve cells in hippocampus and reducing of hydrogen sulfide contents in blood serum. The apoptosis level of hippocampus nerve cells might be concern with the decreasing of endogenous hydrogen sulfide.
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