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| 1 | Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats显示文摘AIM: To investigate effects of ischemic pre-conditioning on the liver endogenous oxidant-antioxidant system during ischemia/reperfusion injury.METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into sham-operated (Sham), ischemia/reperfusion (I/R), ischemic pre-conditioning plus ischemia/reperfusion (IPC) groups. Serum ALT, AST and hyaluronic acid levels were assayed and pathologic alterations observed. Liver malondialdehyde (MDA) contents,endogenous antioxidant enzymes, superoxidase dismutase (SOD), catalase (CAT), gultathionine peroxidase (GSH-Px)activities, neutrophils accumulation marker, myeloperoxidase (MPO) activities were measured respectively.RESULTS: Compared with I/R group, sinusoidal endothelial cells as well as hepatocytes damages, as assessed biochemically and histochemically, were improved significantly in IPC group; neutrophils infiltration was also markedly reduced. In IPC group, liver peroxidation, as measured by MDA contents, was significantly decreased when compared with I/R group; endogenous antioxidant enzymes, SOD, CAT and GSH-Px activities were markedly higher than that in I/R group.CONCLUSION: Ischemic pre-conditioning exerts protective effects on both hepatic sinusoidal endothelial cells and hepatocytes during liver I/R injury. Its mechanisms may involve dimunition of neutrophils infiltration and modulation of the imbalance of endogenous oxidant-antioxidant system in the organism. | Guang-JinYuan Jin-ChunMa Zuo-JiongGong Xiao-MeiSun Shi-HuaZheng XiLi | 2005 | World Journal of Gastroenterology2005，11，12： | 20 |
| 2 | 肝移植缺血再灌注对肝内胆管上皮细胞损伤机制的研究现状显示文摘目的了解肝缺血再灌注(Ischemia and Reperfusion,IR)对人肝内胆管上皮细胞(human Intrahepatic Biliary Duct Cells,hIBDC)损伤机制的研究背景和现状,指导临床相关研究,为深入探讨损伤机制找准切入点,为临床防治提供参考。方法计算机检索PubMed(1970~2007)、中国生物医学文献数据库(CBM,1979~2007),限中英文研究。由两位作者参与文献筛选、资料提取,基于纳入文献性质,分主题作描述性系统评价。结果移植肝IR损伤的研究最早见于1970年,此后逐年增加。共纳入符合纳入标准的文献65篇,含临床研究13篇,基础研究35篇,综述17篇。基础研究以机制研究为主,主要集中在:①胆道与胆管上皮细胞生理;②肝移植IR致IBDC损伤机制;③主要损伤机制包括冷缺血、热缺血、再灌注、胆汁和疏水性胆盐损伤。临床研究主要集中在临床预防研究,包括非手术方法(如灌注液、中药和左旋赖氨酸)及手术方法;临床治疗无重大突破,局限于保守治疗和失败后手术补救。结论①大小hIBDC形态、功能、状态的异质性和肝内外胆道血供的特殊性是IR致胆道损伤的重要物质基础。②笔者发现单纯IR或缺氧再给氧(H/R)可致hIBDC的MHC、MIC、DR4、DR5及各种黏附分子改变。③hIBDC和人肝细胞(human hepatocytes,hHC)相比,不耐冷缺血,更不耐再灌注损伤。④疏水性胆盐能加剧器官保存过程中人、猪胆道系统的损害。⑤由于临床研究文献不多,基线条件和评价指标不统一,结果不能合并,基于目前已有文献,证据强度不够,结论仅供参考。 | 庞丽丽 冯莉 赵娜 李胜富 李璐璐 李永胜 龙丹 李幼平 | 2008 | 中国循证医学杂志2008，8，6： | 7 |
| 3 | 预防肝脏缺血再灌注损伤的研究现状显示文摘 | 崔巍 熊奇如 | 2005 | 中国实用外科杂志2005，25，10： | 6 |
| 4 | Protective effects of glutamine preconditioning on ischemia-reperfusion injury in rats显示文摘BACKGROUND:Hepatic ischemia-reperfusion injury is a common phenomenon in hepatic surgical procedures and can result in further severe damage.This study aimed to investigate the protective effects of glutamine preconditioning on hepatic ischemia-reperfusion injury in rats and its dose-dependency. METHODS:Thirty-two healthy male Wistar rats were randomly divided into four groups(n=8 per group).One group received 0.9%NaCl(control)and the other three received glutamine(Gln groups)4 hours before ischemia.The Gln groups were named GL,GM,and GH according to the glutamine dose.The liver was subjected to 1 hour of ischemia and 2 hours of reperfusion. Two hours later,the levels of alanine aminotransferase(ALT), intracellular free calcium(Ca 2+ ),and activity of Na + /K + adenosine triphosphatase(ATPase)and superoxide dismutase (SOD)were assessed,and liver tissue sections were examined under a microscope. RESULTS:The Gln and control groups differed in the concentration of intracellular free calcium(P<0.05),and the activity of Na + /K + ATPase and SOD in the Gln groups was higher than in the control group(P<0.05).The ALT level was lower in the GM and GH groups than in the control group(P<0.05).The levels of Na + /K + ATPase and SOD rose gradually with increasing glutamine dose(P<0.05),and the concentration of Ca 2+ declined gradually with increasing glutamine dose(P<0.05).The degree of hepatocyte injury was milder in the Gln groups than in the control group. CONCLUSIONS:Glutamine preconditioning protected effectively against hepatic ischemia-reperfusion injury.These protective effects were related to the dose of glutamine and due to the reduction of intracellular calcium overload and the improvements in the activity of Na + /K + ATPase and SOD. | Wan-Xing Zhang,Li-Fang Zhou,Lei Zhang,Lei Bao,Chun-ChengWang,Hui-Yan Meng and WenYin Department of Hepatobiliary Surgery,and Department of Pharmacy ,Hebei Provincial General Hospital,Shijiazhuang 050051,China | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，1： | 5 |
| 5 | 抗氧化剂在降低肝缺血再灌注损伤中的作用显示文摘肝移植、肝部分切除、缺血性休克等往往引起临床上肝脏缺血再灌注损伤,在这些过程中一个显著的特征就是氧化应激反应的发生并伴有内源性抗氧化剂的缺失。机体内复杂的抗氧化系统包括细胞内的酶类或非酶类的自由基清除剂以及饮食中的物质等。采用抗氧化剂治疗可以降低肝缺血再灌注损伤,并且当某些外科策略如缺血预处理不能实施时,药物治疗就显示出独特的优势。近年来,在肝缺血再灌注损伤治疗上有一些新的发展,如超氧化物歧化酶衍生物、含巯基化合物、选择性一氧化氮合酶抑制剂的出现及基因治疗等,多在一定程度上降低了肝缺血再灌注损伤的程度。 | 高元兴 秦华东 刘冬冬 虞焰 | 2009 | 中国组织工程研究与临床康复2009，13，5： | 5 |
| 6 | 谷氨酰胺对肝门阻断后肝脏损伤影响的实验研究显示文摘目的:探讨谷氨酰胺(Gln)对肝门阻断后肝脏损伤的影响及其意义。方法:雄性Wistar大鼠,随机分为3组:假手术组(1组)、对照组(2组)和实验组(3组)。采用Pringle′s法进行肝门阻断,持续35 min,肝门阻断前3组大鼠腹腔注射Gln。分别于肝门阻断前及再灌注后2、4、24 h,每组各选取10只大鼠,测定血清ALT、AST、LDH含量;肝组织谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量,检测血清TNF-α及门静脉血浆内毒素水平。结果:与对照组相比,再灌注后实验组肝组织中MDA含量下降(P<0.05),而GSH及SOD水平增高(P<0.05);血清ALT、AST、LDH含量,TNF-α及内毒素水平均明显降低(P<0.05)。结论:Gln能有效地减轻肝门阻断所致的肝缺血再灌注损伤,可能与Gln抑制内毒素易位及炎症因子释放有关。 | 刘国平 朱闻溪 杨广顺 周文平 程广明 | 2007 | 中国误诊学杂志2007，7，13： | 3 |
| 7 | 谷氨酰胺对大鼠肝脏缺血再灌注损伤时肝组织谷胱甘肽含量和Bcl-2、Bax蛋白表达的影响显示文摘目的:探讨谷氨酰胺(glutamine,Gln)对大鼠肝脏缺血再灌注损伤(HIRI)时肝组织谷胱甘肽(glutathione,GSH) 含量和细胞凋亡相关基因Bcl-2和Bax蛋白表达的影响.方法:将48只健康♂Wistar大鼠随机分为谷氨酰胺组 (G组)和对照组(C组).预置中心静脉导管后经此输液通道分别注入谷氨酰胺溶液和生理盐水行预处理 (3 d).采用Pringle法夹闭肝十二指肠韧带致肝脏缺血 30 min后,去夹恢复血流为再灌注.分别于再灌注后 1、24 h抽血检测ALT的水平,然后快速切取肝组织检测其还原型GSH的含量,切取部分肝组织用于组织病理学检查,并采用S-P免疫组织化学染色方法检测肝组织细胞凋亡相关基Bcl-2和Bax的蛋白表达情况.结果:再灌注后1、24 h,G组血清ALT水平皆显著低于C组(8.3±2.0 μkat/L vs 13.7±5.5 μkat/L,P<0.05; 2.9±2.5 μkat/L vs 9.1±4.3 μkat/L,P<0.01).肝脏组织GSH的水平:再灌注后1、24 h,G组肝组织GSH水平皆明显高于C组(1216.09±152.78 μg/g vs 856.68± 117.64 μg/g,P<0.01;899.73±57.75 μg/g vs 800.50± 94.79 μg/g,P<0.05).肝组织损害的病理学改变:G组明显轻于C组.再灌注后1、24 h,G组肝组织Bcl-2蛋白阳性表达率明显高于C组(100.0% vs 37.5%,P<0.05; 87.5% vs 25.0%,P<0.05);再灌注后1、24 h,G组肝组织Bax蛋白阳性表达率明显低于C组(25.0% vs 87.5%,P<0.05;25.0% vs 87.5%,P<0.05).结论:Gln对大鼠HIRI具有保护作用,其作用机制可能与维持体内GSH含量和影响肝组织细胞凋亡相关基因 Bcl-2和Bax蛋白的表达有关. | 贾昌俊 戴朝六 张旭 徐锋 崔凯 许永庆 | 2005 | 世界华人消化杂志2005，13，19： | 3 |
| 8 | 谷氨酰胺对手足口病合并肝损伤的保护作用显示文摘目的观察谷氨酰胺对手足口病并发肝损伤的肝保护作用。方法将28例手足口病并发肝损伤患儿随机为治疗组和对照组,每组14例,两组均给予常规治疗,治疗组加服复方谷氨酰胺肠溶胶囊,对照组给予还原型谷胱甘肽注射液静滴,疗程均为2周,比较两组治疗前后肝功能指标的变化。结果两组治疗前ALT、AST、ALP水平比较,差异无统计学意义(P>0.05);与治疗前比较,治疗后两组患者ALT、AST水平均下降(P<0.05),但治疗组降低水平显著优于对照组(P<0.05);两组治疗后ALP水平无明显下降(P>0.05)。治疗组、对照组治疗总有效率分别为85.7%和50.0%,治疗组疗效优于对照组(P<0.05)。结论谷氨酰胺对手足口病并发肝损伤有一定的保护作用。 | 李翀 黄波 李柏 | 2015 | 广西医学2015，37，10： | 2 |
| 9 | 门静脉阻断下自制在体冷灌注液对肝脏保护作用的研究显示文摘目的研究经门静脉在体灌注自制灌注液对长时间门静脉阻断下肝脏的保护作用。方法采用人造血管,在肠系膜上静脉、肝下下腔静脉间架桥,建立猪临时性肠腔分流模型。21头巴马猪分3组,门静脉阻断2 h,A组不灌注、B组灌注乳酸林格液、C组灌注自制灌注液,监测各组动物术中HR、MAP,对比观察3组动物2 w存活率,在阻断前、复流前、复流2 h、术后1、3、5 d检测ALT、AST、TBIL的变化;对应时相点切取肝组织,在光镜、电镜下观察肝脏病理变化。结果 3组动物存活率均为100%,C组ALT、AST、肝组织形态学变化明显较A、B两组轻。结论自制保护液能安全进入体循环。经门静脉在体灌注自制灌注液对因门静脉血流长时间阻断导致的肝缺血再灌注损伤具有良好的保护作用。自制灌注液的肝保护作用明显优于乳酸林格液。 | 黄波 别平 | 2012 | 西南国防医药2012，22，1： | 0 |
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