本文關(guān)鍵詞：低氧預適應(yīng)減輕大鼠缺血—再灌注腦損傷中凋亡及相關(guān)蛋白表達的變化　出處：《山西醫(yī)科大學》2006年碩士論文　論文類型：學位論文

  更多相關(guān)文章： 腦缺血 再灌注損傷 低氧預適應(yīng) 凋亡 Survivin fas/fas-L HSP-70

【摘要】： 目的:探討低氧預適應(yīng)減輕大鼠缺血-再灌注性腦損傷中,凋亡及相關(guān)蛋白和HSP70表達的變化。 方法:采用SD大鼠局灶性腦缺血再灌注模型(transient middle cerebral artery occlusion,MCAO),將48只大鼠隨機分為3組6個亞組:假手術(shù)組(Sham)、缺血再灌注組(ischmia/reperfusion I/R)、低氧預適應(yīng)組(hypoxic preconditioning HP+I/R),應(yīng)用免疫組織化學和細胞死亡原位末端標記(Insitu end labeling ,ISEL)法研究腦組織細胞凋亡及凋亡相關(guān)蛋白Survivin、fas/fas-L和應(yīng)激蛋白HSP-70的表達情況;并在缺血(ischemia,I)和再灌注(reperfusion,R)I/R后不同時間點(I1h、I2h、I3h、R1h、R4h、R8h、R24h)對大鼠進行神經(jīng)體征的觀察,記錄動物神經(jīng)行為缺陷計分,通過Y-電迷宮測試缺血再灌注24h后大鼠學習、記憶能力。 結(jié)果: (1)缺血3h再灌注24h后神經(jīng)功能缺陷計分及Y-電迷宮測試大鼠學習記憶能力(N代表學會標準時的訓練次數(shù);A/10代表記憶保持率): Sham組: 0分,N為47.5±7.1 , A/10為0.91±0.08; I/R組: 1.1±0.6分,N為86.3±9.2, A/10為0.54±0.14; HP+I/R組: 0.4±0.5分,N為66.3±7.4, A/10為0.66±0.09。 (2)高倍視野(high power field ,HPF)下Survivin蛋白陽性細胞數(shù): Sham組為0.6±0.9個/HPF,I/R組為14.0±2.1個/HPF, HP+I/R組為27.1±4.2個/HPF。 (3)高倍視野下fas蛋白陽性細胞數(shù): Sham組為0.8±1.2個/HPF,I/R組為27.3±2.8個/HPF, HP+I/R組為11.1±2.2個/HPF。 (4)高倍視野下fas-L蛋白陽性細胞數(shù): Sham組為0.5±0.8個/HPF ,I/R組為24.6±3.6個/HPF, HP+I/R組為9.6±1.7個/HPF。 (5)高倍視野下HSP-70蛋白陽性細胞數(shù): Sham組為0.3±0.5個/ HPF,I/R組為26.3±3.6個/HPF, HP+I/R組為47.0±3.1個/HPF。 (6)高倍視野下凋亡細胞數(shù): Sham組為0.5±0.7個/HPF,I/R組為39.4±2.4個/HPF, HP+I/R組為23.1±4.4個/HPF。 高倍視野下Survivin、fas/fas-L和HSP-70蛋白陽性細胞數(shù)、凋亡細胞數(shù)比較,HP+I/R組與I/R組及Sham組間差異具有統(tǒng)計學意義(p0.05)。缺血3h再灌注24h后神經(jīng)功能缺陷計分及Y-電迷宮測試大鼠學習記憶能力,HP+I/R組優(yōu)于I/R組,差異有統(tǒng)計學意義(p0.05)。 結(jié)論:低氧預適應(yīng)可減輕局灶性缺血再灌注腦損傷,減少大鼠腦缺血再灌注后的腦細胞凋亡和神經(jīng)功能缺失,提高動物學習記憶能力和損傷后神經(jīng)功能恢復。上調(diào)神經(jīng)細胞中Survivin、HSP-70蛋白表達;下調(diào)fas/fas-L蛋白表達可能是其發(fā)揮保護作用的分子機制之一。
[Abstract]:Aim: to investigate the changes of apoptosis and the expression of related proteins and HSP70 in hypoxic preconditioning rats. Methods: transient middle cerebral artery occlusion was used in SD rats with focal cerebral ischemia-reperfusion. MCAO, 48 rats were randomly divided into 3 groups and 6 subgroups: sham-operated group and ischemia-reperfusion group. Hypoxic preconditioning HP I / R in hypoxic preconditioning group. In situ end labeling was labeled by immunohistochemistry and in situ end labeling of cell death. The expression of apoptotic and apoptosis-related protein survivin fas-L and stress protein HSP-70 was studied by ISELL method. At different time points after I / R / R / R, I _ 1h ~ I _ 2h ~ I _ 3h ~ (1) ~ (1h) ~ (1) h ~ (4h) ~ (4) h ~ (8) h ~ (8 h) after ischemia / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion / reperfusion. The neurological signs of rats were observed at 24 h, and the scores of neurobehavioral defects were recorded. The learning and memory abilities of rats after 24 hours of ischemia reperfusion were tested by Y- electrical maze. Results: 1) after 3 h of ischemia and 24 h after reperfusion, the scores of neural function defect and the training times of learning and memory ability in Y- electrical maze test were measured on behalf of the standard of learning. In Sham group, N was 47.5 鹵7.1, A / 10 was 0.91 鹵0.08; I / R group: 1.1 鹵0.6 min N was 86.3 鹵9.2, A / 10 was 0.54 鹵0.14; HP I / R group: 0.4 鹵0.5 min N 66.3 鹵7.4, A / 10 0.66 鹵0.09. (2) the number of Survivin protein positive cells in high power power field (Sham) group was 0.6 鹵0.9 / HPF. The I / R group was 14.0 鹵2.1 / HPFs, and the HP / I / R group was 27.1 鹵4.2 / HPFs. The number of fas protein positive cells in Sham group was 0.8 鹵1.2 / HPFN / I / R group (27.3 鹵2.8 / HPF). The HP I / R group was 11.1 鹵2.2 / HPF. (4) the number of fas-L protein positive cells in the Sham group was 0.5 鹵0.8 / HPF-I / R group (24.6 鹵3.6 / HPF). The HP I / R group was 9.6 鹵1.7 / HPF. (5) the number of HSP-70 protein positive cells in Sham group was 0.3 鹵0.5 / HPF-I / R group 26.3 鹵3.6 / HPF. The HP I / R group was 47.0 鹵3.1 / HPFs. (6) the number of apoptotic cells in the high power field: 0.5 鹵0.7% HPF / R group was 39.4 鹵2.4% HPF in Sham group. The HP I / R group was 23.1 鹵4.4 / HPFs. The number of survivin fas-l and HSP-70 protein positive cells and the number of apoptotic cells were compared in high power field. The difference between HP / I / R group and I / R group and Sham group was statistically significant (p 0.05). After 3 hours of ischemia and 24 hours of reperfusion, the scores of nerve dysfunction and the learning and memory ability of rats were measured by Y- electrical maze. HP I / R group was better than I / R group, the difference was statistically significant (p 0.05). Conclusion: hypoxia preconditioning can reduce focal ischemia-reperfusion injury, reduce brain cell apoptosis and neural function loss after cerebral ischemia-reperfusion in rats. The expression of survivin HSP-70 protein in nerve cells was up-regulated by improving the ability of learning and memory and the recovery of nerve function after injury. Down-regulation of fas/fas-L protein expression may be one of its protective molecular mechanisms.
【學位授予單位】：山西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2006
【分類號】：R363

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