| IntroductionDiabetes mellitus ( DM) and cerebral ischemical reperfusion injury ( CIRI) are important risk factors of cognitive handicap. Hippocampus plays an important role in learning, and memory. Cognitive handicap is closely related to neuronal degeneration, necrosis, deletion in hippocampus. Neuronal apoptosis and cognitive handicap were seen in Dm and CIRI. Many toxic substances take part in this kind of injury. Some report showed that Fas was important risk factor in apoptosis cascade reaction (ACR) , which took part in Dm and CIRI hippocampus injury and Tau also took part in Dm and CIRI hippocampus injury. We want to find the role of Fas, Tau in Dm combined CIRI. We adopt STZ - induced and line lock method to set up CDM - MCAO model. By immunohistochemical and HE techniques, the delayed neuron death and expression of Fas and Tau respectively in Dm group and CIRI group. We want to find their relationship in order to provide clinic the more basis.Materials and methodsA total of 70 - wister rats aged 2-3 months weighting 100 - 130g,randomly divided into 4 groups: â‘ normal control group (n=5) â‘¡ sham operated group (n=5) â‘¢ ischemic - reperfusion (IR group) (n=5) â‘£ diabetes mellitus combined with cerebral ischemical reperfusion group (Dm group) (n=5)â‘¢ -â‘£ groups consisted of 6 groups including 1d ,2d ,3d ,4d ,5d ,7d respectively. DM model: STZ was used in intraperitioneal injection in Rats and cerebral ischemia were made by using line - luck method. Rats whose blood sugar on an empty stomach > 16.7mmol/L was determined to Dm Rats. Dm Rats were bread in 40 day. CIRI model was introduced by Zea Longa. CIRI time was respectively at 1d, 2d, 3d, 4d, 5d, 7d. At various time after ischemical, animals were deeply anesthetized with 10% .chloral Hydrate and perfused by intra-cadiac puncture using 4% poly foraiald chydet, then fixation, cera, embed, serial setion, HE stain and immunohistochemical of Fas, Tau. Semi - guantitative method was applied to analysis neuronal numbers in hippocampus and immunohistochemical cells of Fas, Tau. All redues were stated at mea, comparions between CIRI group and Dm group at different time.ResultDelayed neuron death and up - regulation of Fas and Tau were seen in CAl area of hippocampusus in Dm group, begining at 2d ,high - peak at 4d,decline at 7d, which is more statistically significant than that in cerebral reperfusion group. ( p <0.05)DiscussionDiabetes mellitus and cerebral ischemical reperfusion injury are important risk factors of cognitive handicap. Hippocampus plays an important role in learning and memory. Cognitive is closely related to neuronal degeneration, ner-osis, deletion in hippocampus. We found that CIRI was increased in DM combined CIRI. We think many factors involved in this injury, such as the toxic effect of hyperglycemia, cerebral blood stream declination, absence of insuline, care -action neuropeptide declination, and other toxic substances. By the study of Fas and Tau expression in DM combined with CIRI, we want to find injury mechanism of DM combined with CIRI.We found more Fas activity in DM group which is more than that in CIRIgroup, and Fas as a messager of apoptosis taking part in DM combined with CI-RI. Many factors were involved in this process, such as hyperglycemia, cytor-estc, oxidootive stress, free radical, decrease of insulin, insulin - like growth factor and so on. This showed that hyperglycemia and absence of insulin in crease the Fas activity, which is one of injury mechanism of DM combined CI-RI.Points involved in this injury, such as the toxic effect of hyperglycemia, cerebral blood stream declination, absence of insulin, care - action neuropeptide declination, and other toxic substances. By the study of Fas, Tau expression in DM combined with CIRI, we want to find injury mechanism of DM combined with CIRI.We found, abnormal phosphorylation of Tau in DM group is paralled with the decline of hippocampus neuron, and Fas changes in DM group, which is more reinforcemant than that in CIRI group. We suspected that absence of insulin lead to the abnormal phosphorylation of Tau and hyperglycemia increase the noxious stimulation of Tau. This showed Tau neurotoxic effect was increased by DM, which is one of injury mecharism of DM combined with CIRI.Simply put, at hyperglycemia and absence of insulin, Fas, Tau took part in the injury process of DM combined with CIRI. We suspected that the call - apoptosis mechanism induced by Fas and the neurotoxic effect of Tau were one of injury mechanism of Dm combined with CIRI, which is new idea to the occurrence of cognitive handicap at early time in DM combined with CIRI and provided the new counter measure to the treatment of severity cognitive handicap.Conclusion1. Delayed neuron death was occurred after focal cerebral ischemical reper-fusion in Rats with Dm Which is an important risk factor in cognitive handicap of cerebral ischemia.2. The apoptosis mechanism induced by Fas is one of more Hippocampusus neuron injury effect after cerebral ischemic in Rats with Dm.3. The neurotoxic effect of Tau is one of more hippocampus injury mecha-... |
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