本文選題：鋅　切入點(diǎn)：脊髓缺血再灌注損傷　出處：《吉林大學(xué)》2015年碩士論文　論文類型：學(xué)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(dòng)脈等手術(shù)過程中導(dǎo)致脊髓缺血引起脊髓的損傷，是胸腹主動(dòng)脈手術(shù)和脊柱外科的嚴(yán)重并發(fā)癥之一。目前針對(duì)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(guān)注和亟待解決的重點(diǎn)。相關(guān)研究表明，鋅是機(jī)體的必需微量元素，是機(jī)體多種酶的必要成分或活化因子。參與多種信號(hào)通路的轉(zhuǎn)導(dǎo)，具有抗炎癥抗氧化和抗纖維化等作用。本研究首先對(duì)大鼠進(jìn)行外源性鋅離子補(bǔ)充，然后制備大鼠SCII動(dòng)物模型，觀察其發(fā)生SCII的情況，進(jìn)而探討鋅離子對(duì)脊髓缺血再灌注損傷的保護(hù)性作用并初步探討其作用機(jī)制。 目的探討外源性補(bǔ)鋅對(duì)脊髓缺血再灌注損傷大鼠的保護(hù)作用，并且初步探討其作用機(jī)制。 方法60只Wistar大鼠隨機(jī)分為5組，每組12只，雌雄各半，分別為假手術(shù)組、模型組、硫酸鋅預(yù)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(shù)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(dòng)物模型，損傷后48h采用Tarlov評(píng)分對(duì)脊髓缺血再灌注損傷模型進(jìn)行后肢神經(jīng)功能評(píng)價(jià)；HE染色進(jìn)行病理組織學(xué)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(biāo)志物Beclin1在脊髓組織中的表達(dá)。 結(jié)果與模型組比較，各給鋅組大鼠神經(jīng)功能評(píng)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(xiàn)，脊髓缺血再灌注組部分神經(jīng)元受損，硫酸鋅處理組細(xì)胞形態(tài)均有一定改善。Beclin1免疫組織化學(xué)染色顯示，各干預(yù)組中，25mg/kg/d組和50mg/kg/d組Beclin1蛋白表達(dá)顯著高于假手術(shù)組（P 0.05），各干預(yù)組Beclin1蛋白表達(dá)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(shù)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(shù)組（P＜0.05）。模型組和各硫酸鋅處理組大鼠脊髓組織內(nèi)的MAO活性均顯著高于假手術(shù)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(nèi)的T-AOC含量顯著低于假手術(shù)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(jié)論補(bǔ)充鋅離子可提高大鼠神經(jīng)功能評(píng)分，增強(qiáng)其抗氧化應(yīng)激能力，減少病理組織損傷，對(duì)脊髓缺血再灌注損傷起到一定保護(hù)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(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R651.2

【參考文獻(xiàn)】

相關(guān)期刊論文 前8條

1 馬國強(qiáng);李躍榮;;心肌缺血/再灌注損傷與細(xì)胞凋亡的機(jī)制及其防治研究進(jìn)展[J];濱州醫(yī)學(xué)院學(xué)報(bào);2007年01期

2 馬玉羨;腦缺血再灌注損傷病理生理機(jī)制研究進(jìn)展[J];河南醫(yī)學(xué)研究;1998年04期

3 管華清,顧曉暉,楊惠林,唐天駟;熱休克蛋白對(duì)脊髓缺血再灌注損傷的保護(hù)作用[J];脊柱外科雜志;2004年06期

4 蒙革,朱朗標(biāo),余翼飛,王冬青,朱光明;缺血預(yù)處理對(duì)脊髓缺血兔后肢神經(jīng)功能的影響[J];中華老年心腦血管病雜志;2000年03期

5 郭來敬,張志仁,陳東輝,王璞;電子順磁共振檢測心肌缺血再灌產(chǎn)生的氧自由基及其保護(hù)的實(shí)驗(yàn)研究[J];心肺血管病雜志;2000年01期

6 ;Moderate hypothermia prevents neural cell apoptosis following spinal cord ischemia in rabbits[J];Cell Research;2005年05期

7 王強(qiáng),熊利澤,陳紹洋,桑韓飛,朱正華,董海龍;川芎嗪對(duì)兔脊髓缺血/再灌注損傷的保護(hù)和治療作用[J];中華麻醉學(xué)雜志;2001年03期

8 楊小玉,朱慶三,趙立君,孫慶,秦彥國,段德生;脊髓缺血-再灌注損傷細(xì)胞間粘附分子-1及白細(xì)胞介素-1β的表達(dá)[J];中國脊柱脊髓雜志;2004年03期

本文編號(hào)：1615831