| PrefaceStroke is one of the leading cause of death in the population,with many survivors being left with physical and mental disabilities. Great attention has been always paid to treatment of ischemic cerebral vascular disease. But there are currently limited treatment options for most type of stroke. The treatment of dissolving thrombus is the most promising meathod but yet have some defect which prevent it from being widly performed. Therefore, to study the protectic mechanism following ischemic stroke may become a new meathod to protect the neurons. The GFAP is a specific marker of astrocyte, its expression is more higher in the activity astrocyte, and finally the GFAP become the main composition of scar formations. The S -100 is a kind of acidity, dissolubilites, low molecular quantity and calcium hydronium conjugated protein, and it is mainly existed in neuroglial cell and schwann cell. It can promote the growth of axon, glial hyper-plasia and nerve divide and calcium's stability inside of cell, thus regulating the shape and metabolism of astrocyte . The quantity of S -100 protein and the degree of ischemia have direct proportion . GFAP and the S - 100 protein all show the notable expression at acute cerebral ischemia.ObjectiveTo examinate the expression of GFAP and S - 100 protein between cerebral infarction and diabetes combined cerebral infarction by immunohistochemistry method. To detect the expression of GFAP and S -100 protein in diabetes.Materal and MethodAdult male Sprague - Dawley rats (220 -260g,n = 16) were housed in the same animal care facility during a 12h light/dark cycle throughout the protocol. The animals are divided into 3 expreimental groups sham control group(n =4) , simple focal cerebral infarction group (n =6) , cerebral infarction combined with diabetes group (n =6). The model of diabetic rat: 2%STZ injection into abdomen by 60mg/kg, blood suger is higher than 16. 7mmol/L ,feed for 6 weeks, becomes the model of chronic diabetic rats. Induction of focal cerebral infarction with an filament. Animals were anesthelized with 10% chlorinealdehyde by 0. 3ml/100g. MCA occlusion was induced with an intraluminal filament model as described earlier. Briefly, a filament (4-0 nylon suture) was inserted into the left external cervical artery and lodged in the narrow proximal anterior cerebral artery, blocking the MCA at its origin. Animals were awake during the 2h MCA occlusion. Neurologic deficits in rats were examined after 24h ischemia. The deficits were scored on a modified scoring system developed by Zea. Unable to extend the contralateral forelimb, flexion of contralateral forelimb, mild circling to the contralateral side, severe circling to the contralateral side are considered to be succeeded. After 24h of MCA occlusion animals were deeply anesthelized with 10% chlorinealdehyde and killed by cardie perfusion of saline followed by 4% paraformaldehyde in 0. 1M phosphate buffer. Sections were cut at a thickness of 7um from 4. 0mm from optic chiasma. Parraffin sectins were stain with normal SABC immunohistochemistry to determine cellular expression of neutro-phic factors GFAP,S -100 protein in respective group. Use a computer assisted microscope and an image analysis system. Statistics were analyzed by t test with significance level at p <0. 05.ResultsThe number of positive cells of the matched control GFAP and S ?100 proteins is little, and distribute sparse cell body is the small triangle, the apophysisis short and thinness. The number of positive cells of GFAP and S -100 protein in cerebral infarction is more than the matched control obviously, and the cell body is big, and the apophysis increase thickly become to grow. In diabetes combined cerebral infarction the number of the positive expression cells of GFAP and S - 100 protein obviously increased, and the cell volume enlarge to show big, obviously, apophysis to rise to as well and obviously prolong, increase thick. The positive expression cells are mainly in the verge of ischemia, to be presented at pec...
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