| Stroke 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 paid to treatment for ischemic cerebralvescular 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 defects which prevent it from being widly performed. Therefore, to stucy the endoprotectic mechanism following ischemic stroke may become a new meathod to protect the neuron. NGF,BDNF are the two main members of neurotrophic family. They play an important role in neuron growing, maturing and synapsic forming. They are detected to increase expression after brain injury such as ischemia, tumor, inflammation and traumor. Many studies have confirmed when ischemic brain damage is happaning either focal or global ischemia that the expression of NGF, BDNF protein is increased in the ischemic region. This indicate the relation between NGF, BDNF and the neuron survival and neuroprotection. After intraveinal or focal brain injection of BDNF, neurologic deficits can be improved, the infarction volume can be decreased. Diabetes is one of the imperil disease to mankind. The pathological changes to big blood vessels in diabetes may lead to cardi-alvesscular and cerebralvessecular complications. Studies have indicated that diabetes can increase the risk to stroke. The incidence of disease with diabetes is 4-10 times to that without diabetes. Diabetes can aggravate the stroke prognosis. The infarction volume combined with diabetes is more larger than that without diabetes. The mechanism is thought to be the metabolic acidosis and excit-abilitic aminophenol toxicity. It still unclear whether the neurotrophic factors play a role in the process. The expression of NGF,BDNF is not reported in is-chemic cerebral infarction combined with diabetes. The aim of this study is to examine the expression of NGF, BDNF in the rat brain after simple focal cerebral infarction as well as after focal cerebral infartion combined with 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: control group(n =4) , simple focal cerebral infarction group ( n = 6 ) , cerebral infarction combined with diabetes group (n = 6 ). The model induction 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. Model of focal cerebral infarction is induced with an filament. Animals were anesthelized with 10% chlo-rinealdehyde 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 internal cervical artery and lodged in the narrow proximal anterior cerebral artery, blocking the MCA at its origin. Animals were a-wake 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 succeed. After 24h of MCA occlusion animals were deeply anesthelized with 10% chlorinealdehyde and killed by cardie perfu-sion 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 neutrophic factors NGF, BDNF in respective group. Use a computer assisted microscope and an image analysis system. Statistics were analyzed by ANOVA analyses with significance level at p <0.05.ResultsThe control group has little expresion of NGF and BDNF. Expresion of NGF and BDNF wer...
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