| Objective:The treatment for cerebral ischemia reperfusion (CIR) injury is one of the largest problem nowadays in the worldwide .The trauma of neuron is the mainly reason. Pathophysiological changes induced by CIR injury were proved to be fairly complicated in great numbers of animal and clinical experiments. These pathophysiological changes were intimately correlated with many factors, such as:production of free radical, intracellular calcium overload and so on. The neuron to be closely dead was saved during the CIR injury, on the other hand the trauma to neurons was aggravated. The study suggested that endogenous nervous protection mechanisms had been started during the happening of CIR injury. These mechanisms were included by neurotrophic factor(NTF)introduction and delivering inhibitory transmitter and so on. Insulin-like growth factor-1, as one of the most important growth factors in human are abundant in CNS. During the development and growth of CNS, it is an essential polypeptide composed by 70 amino acids. It can improve the function of nerve cells by protecting the damaged tissue and decreasing the degree of damage in CNS.The special receptor, IGF-1 R is necessary for the function. Extensive existence of IGF-1 R in Purkinje cells and granular cells of cerebral cortex in adults and its lasting expression in brain regions abundantly containing the above nerve cells, which clarifies that IGF-I R has an important role in the mature CNS.The research topic is aim to study the expression of insulin-like growth factor-1(IGF-1)in focal cerebral ischemia reperfusion injury on rat, the brain water content changes on different time points and its (IGF-1)contribution to expression in rats after middle cerebral artery occlusion(MCAO).IGF-1's nervous protection mechanism was explored as well.Methods:A total of 72 adult male Sprague-Dawley rats were subjected to MCAO,and they were randomly divided into sham group,CI group and CIR group.Each group consisted of 5 subgroups(6 h,24 h,48 h,72 h and 7d),according to different time points, post-ischemia, The neurological deficit score(NDS)was assessed with 4 different methods, brain water content measured using the wet-dry method. Histopathology changes observed with HE staining, IGF-1 expression detected by immunohistochemistry. The focal cerebral ischemia rat models were induced using the filament method, the expressions of IGF-1 protein and was detected by the method of immunohistochemical staining.Results:There are 17 rats dead, then rats randomly added up to 72 rats.①The brain water content both in CI group and CIR group increased obviously at 24h,reached to maximum at 72 h and continued to 7d,Compared with the sham group there was significant difference at all the time points(.P<0.05)②with the peak at 72 h,and continued to 7 d,the inflammatory cell infiltration in the infarction regions.③The ethology score decreased and the histopathologic damages were alleviated with administration.④The expression of IGF-1 was very low in normal tissues, while increased mainly in penumbra after cerebral ischemia. The expressions of IGF-1 protein were 169.64±6.97 and 168.64±6.28,respectively,at 24 h after reperfusion and peaked to 168.86±5.39 and 170.86±5.07 at 48 h after reperfusion.Conclusion:the improved animal model of MCAO is ideal to be used in CIR foundation study. The expression of IGF-1 protein was increased after CIR injury in penumbra. Enhanced expression of endogenous IGF-1 has protective effects on focal cerebral ischemia reperfusion injury.
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