| Chronic diabetes mellitus ( CDM) and cerebral ischemical reperfusion injury (CIRI) are important risk factors of cognitive handicap . Hippocamp plays an important role in learnimg , and memory. Cognitive handicap is closely related to neuronal degeneration, necrosis, deletion in hippocamp Neuronal apoptosis and cognitive handicap was seen in CDM and CIKI. Many toxic substances take part in this kind of injury . Some report showed that Caspase - 3 was a key protease in apoptosis cascade reaction ( ACR) , which took part in CDM and CIKI hippocamp injury and Aβ - also took part in CDM and CIRI hippocamp injury . We want to find the role of caspase - 3, Aβin CDM 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 β - amyloid protein (Aβ)and caspase -3 respectively in DM group and CIRI group. We want to find their relatiouship 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 into4 groups :①normal. control group (n = 5 ) ②sham operated group ( n = 5) ③ischemic - reperfusion group (IR group) ( n = 5) ④chronic diabetes mellitus combined with cerebral ischemical reperfusion group (DM group) ( n =5). ③ -④ groups cou-sisted of 6 groups including 1d,2d,3d,4d,5d,7d. respectively. CDM model; STZ was used in intraperitioneal injection in Rats . and cerebral ischemia were made by using line - lock method.ResultDelayed neuron death and up - regulation of Aβand caspase - 3 was seen in CA1 area of hippocampus in DM group , beginning at 2d , high - peak at 4d , dedine at 7d , which is more statistically significant than that in cerebral reperfusion group, (p <0.05 )Discussionchronic diabetes mellitus ( CDM) and cerebral chemical reperfusion injury ( CIRI) are important risk factorsof cognitive handicap . Hippocamp plays an important role in learing and memory . Cognitive is closely related to neuronal degeneration, nerosis, deletion in hipp-ocamp . We found that CIRI was increased in CDM combined CDM , We think many factors involved in this injuny , such as the toxic effect of hyperglycemia, cerebral blood stream dedincotion, absence of insu-lin , care -action neuropeptide dedintion, and other toxic substances. By the stuy of caspase -3, Apiexpression in CDM combined with CIRI , we want to find injury mechanism of CDM combined with CIRI .We found more caspase - 3 activity in DM group which is more than that in CIRI group , and caspase - 3 as a key enzyme of apopto-sis taking part in CDM combined with CIRI . Many factors was involved in this process , such as hyperglycemia, cytorest C, oxidootive stress, free radical , decrease of insulin , insulin - like growth factor and so on. This showed that hyperglycemia and absence of insulin increase the caspase - 3 activity, which is one of injury mechanism of CDM combined CIRI Rats whose blood sugar on an empty stomach > 16. 7mol. L - 1 was determined to DM Rats . DM Rats was bread in 40 days. CIRI model was introduced by Zea Longa. CIRI time was respectively at 1d, 2d, 3d, 4d, 5d, 7d. At various time after ischemi-a, animals was deeply anesthetized with 10% chloral Hydrate and perfused by intracadiac puncture using 4% poly formald chydet, then fixation , cera, embed, serial setion, HE stain and immunohistochemical of Aβ. caspase. Semi - guantitative method was applied to analysis neuronal numbers in hippocamp and immunohistochemical cells of Aβ. caspase-3 . All radues was stated at mea. comparions between CIRI group and DM group at different time - points of involved in this injury, such as the toxic effect of hyperglycemia, cevebral blood stream declination, absence of insulin, cave - action neuropeptide de-dination, and other toxic substances. By the study of caspase -3 , Aβ expression in CDM combined with CIRI, we want to find injury mechanism of CDM combined with CIRI.We found more caspase - 3 activity in DM gro...
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