本文選題：鋅　切入點：脊髓缺血再灌注損傷　出處：《吉林大學》2015年碩士論文　論文類型：學位論文

【摘要】：脊髓缺血再灌注損傷（SCII）是指在脊柱外科和胸腹主動脈等手術過程中導致脊髓缺血引起脊髓的損傷，是胸腹主動脈手術和脊柱外科的嚴重并發(fā)癥之一。目前針對脊髓缺血再灌注損傷的治療方法雖有一定的作用，但療效并不顯著。因此，如何減輕或避免脊髓缺血再灌注損傷成為人們關注和亟待解決的重點。相關研究表明，鋅是機體的必需微量元素，是機體多種酶的必要成分或活化因子。參與多種信號通路的轉導，具有抗炎癥抗氧化和抗纖維化等作用。本研究首先對大鼠進行外源性鋅離子補充，然后制備大鼠SCII動物模型，觀察其發(fā)生SCII的情況，進而探討鋅離子對脊髓缺血再灌注損傷的保護性作用并初步探討其作用機制。 目的探討外源性補鋅對脊髓缺血再灌注損傷大鼠的保護作用，并且初步探討其作用機制。 方法60只Wistar大鼠隨機分為5組，每組12只，雌雄各半，分別為假手術組、模型組、硫酸鋅預處理高劑量組（100mg/kg/d）、中劑量組（50mg/kg/d）和低劑量組（25mg/kg/d）。各劑量組每日灌胃給予硫酸鋅1次，連續(xù)7天。假手術組和模型組給予相同體積生理鹽水，，7天后制備脊髓缺血再灌注損傷動物模型，損傷后48h采用Tarlov評分對脊髓缺血再灌注損傷模型進行后肢神經功能評價；HE染色進行病理組織學觀察；測定脊髓組織中ATP酶、MAO活性和T-AOC含量。免疫組化方法測定自噬的標志物Beclin1在脊髓組織中的表達。 結果與模型組比較，各給鋅組大鼠神經功能評分明顯高于模型組，差異具有顯著性（P 0.05）。病理組織觀察發(fā)現，脊髓缺血再灌注組部分神經元受損，硫酸鋅處理組細胞形態(tài)均有一定改善。Beclin1免疫組織化學染色顯示，各干預組中，25mg/kg/d組和50mg/kg/d組Beclin1蛋白表達顯著高于假手術組（P 0.05），各干預組Beclin1蛋白表達與模型組相比均有顯著性降低（P 0.05）。各硫酸鋅處理組Na+-K+-ATP酶活性明顯低于假手術組（P＜0.05），但明顯高于模型組（P＜0.05）。模型組和各硫酸鋅處理組脊髓組織Ca2+-Mg2+-ATP酶活性顯著低于假手術組（P＜0.05）。模型組和各硫酸鋅處理組大鼠脊髓組織內的MAO活性均顯著高于假手術組（P＜0.05），且100mg/kg/d硫酸鋅處理組MAO活性顯著低于模型組（P＜0.05）。模型組和各硫酸鋅處理組大鼠脊髓組織內的T-AOC含量顯著低于假手術組（P＜0.05）。模型組大鼠脊髓組織中T-AOC含量最低，隨著硫酸鋅劑量的增加，T-AOC含量呈上升趨勢。 結論補充鋅離子可提高大鼠神經功能評分，增強其抗氧化應激能力，減少病理組織損傷，對脊髓缺血再灌注損傷起到一定保護作用。
[Abstract]:Spinal cord ischemia-reperfusion injury (SCII) refers to spinal cord injury caused by spinal cord ischemia during spinal surgery and thoracoabdominal aorta surgery. It is one of the serious complications of thoracoabdominal aortic surgery and spinal surgery. Although the current treatment of spinal cord ischemia-reperfusion injury has a certain effect, but the effect is not significant. How to reduce or avoid spinal cord ischemia-reperfusion injury has become the focus of attention and urgent need to be solved. Related studies have shown that zinc is an essential trace element in the body. It is an essential component or activator of many enzymes in the body. It is involved in the transduction of many signaling pathways, and has anti-inflammatory, anti-oxidation and anti-fibrosis effects. In this study, we first supplemented the rats with exogenous zinc ions, and then made the rat SCII animal model. To investigate the protective effect of zinc ion on spinal cord ischemia-reperfusion injury and its mechanism. Objective to investigate the protective effect of exogenous zinc supplementation on spinal cord ischemia reperfusion injury in rats and its mechanism. Methods Sixty Wistar rats were randomly divided into 5 groups, 12 rats in each group, half male and half female. They were sham-operated group, model group, high dose zinc sulfate preconditioning group (100 mg / kg / d), middle dose group (50 mg / kg / d) and low dose group (25 mg / kg / d). The spinal cord ischemia-reperfusion injury model was established 7 days after sham-operation group and model group were given the same volume of normal saline for 7 days. 48 hours after injury, the spinal cord ischemia-reperfusion injury model was evaluated by Tarlov score and HE staining was used to observe the histopathology. The activity of ATP enzyme Mao and the content of T-AOC in spinal cord tissue were measured. The expression of Beclin1, a marker of autophagy, was detected by immunohistochemistry. Results compared with the model group, the neurological function scores of each zinc group were significantly higher than those of the model group, and the difference was significant (P 0.05). The pathological observation showed that some neurons were damaged in the spinal cord ischemia-reperfusion group. In zinc sulfate treated group, the cell morphology was improved. Beclin1 immunohistochemical staining showed that, The expression of Beclin1 protein in 25 mg / kg / d group and 50 mg / kg / d group was significantly higher than that in sham operation group (P 0.05). The expression of Beclin1 protein in each intervention group was significantly lower than that in model group (P 0.05). The Na K ATPase activity in each zinc sulfate treatment group was significantly lower than that in sham operation group. The activity of Ca2 mg 2 ATPase in spinal cord in model group and zinc sulfate treatment group was significantly lower than that in sham operation group (P < 0 05). The MAO activity in spinal cord tissue of model group and zinc sulfate treatment group was significantly higher than that of sham operation group. The activity of MAO in the 100 mg / kg / d zinc sulfate treatment group was significantly lower than that in the model group (P < 0.05). The T-AOC content in the spinal cord of the model group and the zinc sulfate treatment group was significantly lower than that in the sham operation group (P < 0.05). The content of T-AOC in the spinal cord of the model group was the lowest. The content of T-AOC increased with the increase of zinc sulfate dosage. Conclusion supplementation of zinc ion can improve the neurological function score, enhance the ability of antioxidant stress, reduce the injury of pathological tissue and protect the spinal cord from ischemia-reperfusion injury.
【學位授予單位】：吉林大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R651.2

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