| For the high incidence, mortality and disability rates, cerebrovascular diseases (CVD) are seriously endangering man's health; it has become one of the three top death reasons in mankind. Epidemic investigations show: the ratio between man and woman is about 1.3:1-1.7:1, but there is no significant difference since postmenopause. In addition postmenopausal women are more vulnerable to neurodegenerative disease, and estrogen replacement therapy obviously attenuates the diseases and the risks. More attention were paid to estrogen's function on central nervous system (CNS) . Researches show estrogen may through multiple mechanisms to reduce the injury of cerebral ischemia-reperfusion. Such as increase cerebral blood flow of the ischemic region, sequester free radical, reduce excitatory amino acid's excitotoxicity by inhibiting NMDA (N-methyl-D-aspartate) directly, and lower the density of free Ca2+ in cells et al. but few researches are about the influence of estrogen on the apoptosis hi cerebral ischemic injury. Apoptosis is the main way of neuron death in cerebral penumbra. The key for CVD therapy is to save the still alive neurons in penumbra. Bcl-2 is one familiar gene that has close relationship with apoptosis, and it can prevent ether necrosis or apoptosis. The expression of Hsp70 is increased when stressed. Its main function is as 'molecular company', that mean it can integrate with the water-sparse region of degeneration proteins to prevent them integrate with each other and release the combined proteins to recover their advanced structure in order to inhibit apoptosis. Apoptosis is executed by activating caspases, which caspase-3 belong to. It is the most important caspase that people have done much effort to it. In addition it's the key proteinase during mammalian apoptosis, so it is also called dead proteinase. The aim of this experiment is to observe of the expression of Bcl-2 ,Caspase-3 , Hsp70 on focal Cerebral ischemia-reperfusion injury in rats when treated with estrogen, demonstrates the estrogen-mediated neuroprotections and elucidate the mechanisms in apoptosis. Materials and methods:Twenty healthy male rats were randomly divided into three groups; namely, sham operation group (n=4) ,pure ischemia-reperfusion injured group(n=8) and estradiol treatment group(n=8) . Dissolved into refined peanut-oil, 17 P -estradiol was sterilized by high temperature and pressure and put away avoid of light, estradiol was injected intraperitoneally (100Mg/kg) to estradiol treatment group daily, seven days before the cerebral middle artery occlusions (MCAO) , the same dose of peanut-oil was administrated to the sham-operation group and pure ischemia-reperfusion injured group samely. Rats' cerebral ischemia-reperfusion injury model was established by reversible inserting a nylon thread method. Assess rat's movements before decapitation. Following 24h's reperfusion the rats were decapitated and made into 2mm coronary sections for TTC-stain to measure the infarction after 2h' s ischemia so that we can see whether the model is success and whether estradiol can reduce infarction.Seventy-two healthy male rats were randomized into three groups, sham operation group (n=8). pure ischemia-reperfusion injured group(n=38) and estradiol treatment group(n=8). The latter two groups were further divided into 3h, 6h, 12h, 24h, and these four time points, according to the reperfusion time. Each time point has 8 rats. Estradiol or peanut-oil was delivered as before, when the time came the rats were decapitated. All the sham operation rats were decapitated for brain 6hs after operation. Assess rat's movements before decapitation, the pruned brains were embed in paraffin wax , Serial coronary sections (4 V- m) were used for immunohistochemistry to detect the protein expression of Bcl-2 Caspase-3 and HSP-70 to explore the mechanisms of estradiol, and some sections were hemotoxylin-esion stained to observe the pathological structure-Results1. The movements of the rats in estradiol treatment group were much better...
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