| Today, there is not ideal treatment on permanent focal cerebral ischemia, seeking effective treatment on cerebral ischemia disease has important clinic significance. The death of hypoxia after cerebral ischemia include death and apoptosis. Cell apoptosis is a kind of complicated process of physiology and pathology. NAC is a kind of important anti - apoptosis drug which has protective action for ischemia cerebral disease. At present the accuate mechamism for NAC treatment cerebral ischemia is not clear. Apoptosis is one of the way to cell death in cerebral ischemia which is the programmed cell death regulated by various agents including genes. Caspase family is a well studied gene related to apoptosis. Caspase family is proteinase which introdces effective and typical protein crystal effect. Caspase has an important role in enlighten and complete in cell apoptosis. Caspase - 1 is called executer of cell apoptosis which is necessary killer proteinase in cell apoptosis process. There were seldom reports about whether the protection of NAC against cerebral ischemia are related to apoptosis and apoptotics gene. Infarct volume,caspase - 1 were detected by making rat model of focal cerebral ischemia intraluminal occlusion of middle cerebral artery. The purpose is to investigate the effect of NAC on apoptosis and relevant mechanism after permanent focal cerebral disease which supply theory proof for clinic use.Materials and Methods1 Group : A total of 70 healthy adult male Sprague - Dawley (SD) rats aged 4-5 months,weighting 250 -290g,randomly divided into 4 group: â‘ normal control group ( n = 5) â‘¡ sham operated group ( n = 5 ) â‘¢ ischemia group â‘£ NAG - treated group â‘¢ -â‘£groups consisted of 6 groups including 24h ,48h,72h, 96h,120h, 7d respectively (n =5)2 Method; Permanent focal cerebral ischemia was induced using intraluminal occlusion of middle cerebral artery introduced by Nagasa-wa et. NAG - group received NAG after middle cerebral artery ischemia in 30 minutes by abnormal. The left group infect natrichloridi 0. 5ml by abnormal. At various times after ischemia (24h,48h,72h, 96h,120h,7d) , animals were deeply anesthetized with 10% chloral hydrate and perfused by intracadiac puncture using 4% poly formaldehyde -0. 01MPBS(PH =7.4). Brain were then excised and postfixted for 24h. Brain tissues were embedded in paraffin, coronally sectioned (6um). The size of infarct on coronal sections of HE staining were measured using Q579 image analysis system. The infarct volume was calculated as the sum of the sectional infarct area multipilied by the interval thickness. Immunohistochemistry ( SP) was used to observe the expression of caspase - 1 protein. Semi - quantitative method was applied to analysis immunohistochemical cells. All values were stated as mean S. D. Comparisons between ischemia - group and NAC -group at different time - points of cerebral ischemia were made using t- test.Result1. Infarct Volum.- The infarct lesion was initially found at 24h of ischemia within the territory of the occluded middle cerebral artery including cortex and subcortical areas with light microscope. The boundaries between areas of ischemia damage and the adjacent normal areas of the brain could be sharply delineated. The infarct volum then e-volved until 24h of ischemia and did not significantly vary from 24h -72h ,but decreased at 120h and 7d. NAG - treated groups decreased the infarct volum significantly compared with that of ischemia groups at different time - points of cerebral ischemia.2. Immunohistochemistry of caspase - 1 protein: There were positive a few staining cells in normal contral group and sham operated group . The caspase -1 protein peaked at 72h, maintained high level at 120h and decreased at 7d. The caspase - 1 positive staining cell were mainly microglia. In NAG - treated groups caspase - 1 positive staining cell deceased at different time - points of cerebral ischemia compared with those of ischemia group at different time points of cerebral ischemia.Disussion... |
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