本文關鍵詞： JNK3 腦損傷 細胞凋亡 神經(jīng)功能恢復　出處：《昆明醫(yī)科大學》2013年碩士論文　論文類型：學位論文

【摘要】：目的：越來越多的證據(jù)表明腦損傷(traumatic brain injury, TBI)后c-Jun氨基末端激酶(c-Jun amino-terminal kinase, JNK)通路的激活參與神經(jīng)細胞凋亡及神經(jīng)功能恢復。然而,其是通過激活JNK家族中哪些基因發(fā)揮作用的呢?目前并不十分明確。因此,我們采取原位末端標記法(TdT-mediated dUTP Nick-End Labeling, TUNEL)、逆轉錄聚合酶鏈式反應(Reverse Transcription-Polymerase Chain Reaction, RT-PCR)、神經(jīng)功能缺損評分(Neurological Severity Scores, NSS)等方法,探討腦損傷大鼠JNK1, JNK2, JNK3基因表達變化、神經(jīng)元凋亡及神經(jīng)功能改變的關系。 方法：取SPF級Sprague-dawly(SD)成年健康6月齡雄性大鼠100只,體質量220-260g,隨機分為假手術組30只和腦損傷組70只(自由落體撞擊法建立腦損傷模型)。RT-PCR檢測：假手術組10只,腦損傷組分為1h組、6h組、1d組和7d組各取10只；損傷周邊區(qū)皮質取材取材進行TUNEL染色：假手術組10只,腦損傷組分為6h組和7d組各取10只；用NSS評分評估神經(jīng)功能的改變：假手術組和腦損傷組各取10只。 結果：發(fā)現(xiàn)大鼠腦組織JNK3基因表達在TBI后1h、6h、1d和7d下降(P0.05),JNK1和JNK2的表達無明顯變化(P0.05)。TUNEL染色顯示：TBI后6h腦損傷周邊區(qū)凋亡細胞數(shù)顯著增多(P0.05),TBI后7d較傷后6h減少(P0.05),腦損傷皮質周邊區(qū)凋亡神經(jīng)細胞逐漸減少。大鼠神經(jīng)功能缺損評分在腦損傷后1,3,5,7,14,28d逐漸降低,各時間點組間比較,差異有統(tǒng)計學意義(P0.05)；TBI組與假手術組比較,NSS評分明顯增加(P0.05)。 結論：JNK3在腦損傷后表達下調(diào),可能與神經(jīng)細胞凋亡相關,JNK3的下調(diào)可能促進腦損傷后神經(jīng)功能的恢復。
[Abstract]:Objective : To investigate the effects of activation of c - Jun amino - terminal kinase ( p - c - Jun amino - terminal kinase ) via activation of c - Jun amino - terminal kinase in brain injury and the restoration of nerve function . However , it is not very clear about which genes are activated in the family of brain injury . Therefore , we have studied the relationship between the expression changes , neuronal apoptosis and nerve function changes in rats with brain injury by means of the method of in - situ end labeling ( tdT - mediated nick - End Labeling , TUNEL ) , Reverse Transcription - Polymerase Chain Reaction ( RT - PCR ) and neurological deficit scoring ( NSS ) . Methods : 100 male rats with SPF grade Sprague - Dawley ( SD ) were randomly divided into sham operation group ( 30 rats ) and brain injury group ( 70 rats ) . Results : There was no significant change in the expression of NK3 gene in brain tissue of rats ( P0.05 ) . The number of apoptotic cells in the peripheral area of brain injury was decreased significantly ( P0.05 ) . Conclusion : The down - regulation after brain injury may be related to neuronal apoptosis , and the down regulation may promote the recovery of neurological function after brain injury .

【學位授予單位】：昆明醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2013
【分類號】：R651.15

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本文編號：1492554