三七总皂甙对大鼠肝缺血再灌注损伤的保护

三七总皂甙对大鼠肝缺血再灌注损伤的保护梁力建１何强２吕明德１彭宝冈１黄洁夫Ｔｈｅｐｒｏｔｅｃｔｉｖｅｅｆｅｃｔｓｏｆｐａｎａｘｎｏｔｏｇｉｎｓｅｎｇｏｎｌｉｖｅｒｉｓｃｈｅｍｉａ－ｒｅｐｅｒｆｕｓｉｏｎｉｎｊｕｒｙｉｎｒａｔｓＬＩＡＮＧＬｉ＿Ｊｉ...     

中药对肝缺血再灌注损伤的防护作用

近年发现,经过一定时间缺血的组织器官在得到血液再灌注时却出现了明显的功能结构障碍,甚至发生不可逆的损伤性变化,称为缺血再灌注损伤(Ischemia Reperfusion Injury)。这种现象在肝脏疾病中可观察到,如复杂的肝切除术、严重肝创伤的处理、肝移植等手术中,称之为肝缺血再灌注损伤(Hepatic Ischemia Reperfusion Injury,HIRI)。目前认为氧自由基及     

不同缺血预处理方案对小鼠肝缺血再灌注损伤的影响

肝脏缺血再灌注（ischemia-reperfusion，I／R）损伤是临床常见的问题，是肝脏手术患者术后恢复慢甚至手术失败的重要原因之一。缺血预处理（ischemic preconditioning，IPC）可减轻肝脏I／R损伤。我们通过比较不同IPC方案对C57BL／6小鼠肝脏I／R损伤的影响，为寻找合理有效的IPC方案提供依据。     

肝缺血再灌注损伤对乳酸脱氢酶活性的变化和川芎嗪的？…

目的：探讨肝缺血再灌注损伤（ＨＩＲＩ）时乳酸脱氢酶（ＬＤＨ）活性的改变及川芎嗪的保护作用。方法：制备ＨＩＲＩ模型，随机将２１只家兔发为三组（对照组，７只，盐水组，７只，川芎组，７只）观察血清及肝组织ＬＤＨ活性的动态变化及川芎嗪对它们的影响，结果：盐水组血清ＬＤＨ活性进行性升高，肝组织ＬＤＨ则明显下降，川芎组变化不明显，血清及肝组织ＬＤＨ活性与盐水组比较，均有显著性差异。结论：川芎嗪对ＨＩＲＩ时ＬＤ     

逆灌注对移植肝缺血再灌注损伤的影响

目的:探讨原位肝移植中经下腔静脉逆行灌注对移植肝缺血再灌注损伤的影响.方法:36例大鼠肝移植随机分为3组,每组12例.门静脉组即经门静脉顺行灌注,肝动脉+门静脉组即同时开放肝动脉及门静脉顺行灌注,下腔静脉组即先吻合下腔静脉后开放逆行灌注,然后吻合门静脉及肝动脉.分别检测术后1、6及24 h的血清转氨酶、移植肝病理变化及...     

肝缺血再灌注损伤与NF-κB

核转录因子-κB(Nuclear Factor-Kappa B,NF-κB)是一种重要的转录因子,近年来的研究表明,在炎症反应、免疫反应及细胞凋亡中起重要作用,在肝缺血再灌注损伤过程中亦至关重要。现就NF-κB及其在肝缺血再灌注损伤过程中的作用机制作一综述。     

组织因子、凝血功能紊乱与肝缺血再灌注损伤

近年来，随着临床治疗技术的发展，使许多组织、器官缺血后重新得到血液灌注，损伤结构得以修复。但在有些情况下，经过一定时间缺血的组织和器官的功能，在得到血流再灌注时，出现了明显障碍，导致原有的缺血性损伤进一步加重或出现新的损伤，即缺血一再灌注损伤（ischemia-reperfusion iniury，IRI）。近年来研究表明，     

大鼠急性缺血性肾衰竭不同时段肾功能变化

目的观察大鼠肾脏缺血/再灌注损伤（IRI）模型不同时段肾功能、肾脏/体重指数变化情况。方法建立大鼠肾脏IRI模型,监测大鼠术后不同时段血清尿素氮（BUN）、肌酐（SCr）、血钾及肾脏/体重指数,了解IRI大鼠肾功能变化情况。结果 （1）术后12 h肾脏/体重指数显著升高,至手术后48 h达高峰,于手术后72 h开始回落。（2）术后6 h血清BUN、SCr、血钾显著升高,至术后48 h达高峰,从术后72 h开始回落。结论 IRI大鼠模型手术后肾脏/体重指数、血清BUN、SCr、血钾均有不同程度的升高,高峰期均在术后48 h,提示肾功能损害最严重是在手术后48 h。     

肝缺血再灌注损伤对肿瘤增殖、转移的影响

肝缺血再灌注损伤(hepatic ischemia/reperfusion injury,HIRI)是肝脏外科常见的病理生理过程.HIRl通过引起趋化因子、黏附分子、基质金属蛋白酶、血管内皮细胞生长因子等细胞因子表达改变,对血液中残留肿瘤细胞的迁移、黏附、定植、生长等步骤有着重要的影响.与肝癌术后的复发、转移关系密切.     

Caspase recruitment domain 6 protects against hepatic ischemia/reperfusion injury by suppressing ASK1

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急性肾缺血再灌注损伤氧化侵袭与细胞凋亡

目的探讨急性肾缺血再灌注损伤过程氧化侵袭与肾细胞凋亡在肾损伤发生机制中的作用。方法采用摘除大鼠左肾,钳夹右侧肾蒂的方法,制成急性缺血再灌注肾损伤模型,测定GSHPx、SOD活性和MDA含量及检测肾细胞凋亡率。结果缺血再灌注不同时期肾组织SOD活力水平降低,与对照组相比差异显著(P<0.05,P<0.01),MDA含量高于对照组(P<0.05),GSHPx在再灌注早期活力减弱,明显低于对照组(P<0.01),晚期活力基本恢复;肾细胞凋亡率与对照组相比差异显著(P<0.05、P<0.01);抗氧化酶SOD活力与细胞凋亡率负相关,MDA含量与细胞凋亡率正相关。结论缺血再灌注不同时期肾组织氧化侵袭在肾损伤病理过程中起重要作用;再灌注损伤与氧化侵袭和细胞凋亡有关。     

Role of P-selectin and anti-P-selectin monoclonal antibody in apoptosis during hepatic/renal ischemia reperfusion injury

AIM To evaluale the potential role of P-selectin and anti-P-selectin monoclonal antibody (mAb) in apoptosis during hepatic/renal ischemiareperfusion injury. METHODS Plasma P-selectin level, hepatic/renal P-selectin expression and cell apoptosis were detected in rat model of hepatic/ renal ischemia-reperfusion injury. ELISA, immunohistochemistry and TUNEL were used. Some ischemia-reperfusion rats were treated with antiP-selectin mAb. RESULTS Hepatic/ renal function insufficiency, up-regulated expression of P-selectin in plasma and hepatic/renal tissue, hepatic/renal histopathological damages and cell apoptosis were found in rats with hepatic/renal ischemiareperfusion injury, while these changes became less conspicuous in animals treated with anti-P selectin mAb. CONCLUSION P-selectin might mediate neutrophil infiltration and cell apoptosis and contribute to hepatic/renal ischemia-reperfusion injury, anti-P-selectin mAb might be an efficient approach for the prevention and treatment of hepatic/renal ischemia-reperfusion injury.     

Effect of peroxisome proliferator-activated receptor gamma agonist on heart of rabbits with acute myocardial ischemia/reperfusion injury

Objective:To explore protective effect of rosiglitazone on myocardial ischemia reperfusion injury.Methods:A total of 48 male SD rats were randomly divided into control group(A),I/R group(B),high dose of rosiglitazone(C),low dose of rosiglitazone(D).Plasm concentration of creatine kinase(CK),CK-MB,hsCRP,Superoxide dismutase(SOD),malondialdehyde(MDA),glutathione peroxidase(GSH-Px),nitric oxide(NO)and endothelin(ET)were measured 1 h later after I/R.24 h after I/R hearts were harvested to observe pathological and ultrastructural changes.Immunohistochemistry and western blotting was used to test CD40 expression in myocardial tissue.Area of myocardial infarction were tested,arrhythmia rate during I/R was recorded.Results:Plasm concentration of creatine kinase(CK),CK-MB,hsCRP,NO,MDA and ET were decreased in group C,D compared with group B.Plasm concentration of T-SOD and GSHPx was increased significantly in group C,D compared with group B.Compared with group B,pathological and ultrastructural changes in group C,D were slightly.Myocardial infarction area and arrhythmia rate were lower in group C,D compare with group B.Conclusions:Rosiglitazone can protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration,inhibit inflammatory reaction,improve endothelial function,reduce oxidative stress and calcium overload.     

Effect of remote ischemic preconditioning on hepatic microcirculation and function in a rat model of hepatic ischemia reperfusion injury

Background:

Liver transplantation involves a period of ischemia and reperfusion to the graft which leads to primary non-function and dysfunction of the liver in 5–10% of cases. Remote ischemic preconditioning (RIPC) has been shown to reduce ischemia reperfusion injury (IRI) injury to the liver and increase hepatic blood flow. We hypothesized that RIPC may directly modulate hepatic microcirculation and have investigated this using intravital microscopy.

Methods:

A rat model of liver IRI was used with 45 min of partial hepatic ischemia (70%) followed by 3 h of reperfusion. Four groups of animals (Sham, IRI, RIPC+IRI, RIPC+Sham) were studied (n= 6, each group). Intravital microscopy was used to measure red blood cell (RBC) velocity, sinusoidal perfusion, sinusoidal flow and sinusoidal diameter. Neutrophil adhesion was assessed by rhodamine labeling of neutrophils and cell death using propidium iodide.

Results:

RIPC reduced the effects of IRI by significantly increasing red blood cell velocity, sinusoidal flow and sinusoidal perfusion along with decreased neutrophil adhesion and cell death.

Conclusions:

Using intravital microscopy, this study demonstrates that RIPC modulates hepatic microcirculation to reduce the effects of IRI. HO-1 may have a key role in the modulation of hepatic microcirculation and endothelial function.     

血红素氧合酶-1与肝脏缺血再灌注

血红素氧合酶(HO)是催化分解血红素生成一氧化碳、胆绿素和二价铁离子的限速酶。近来研究发现,HO-1与肝脏缺血再灌注损伤关系密切,此文从HO-1抗氧化、抗凋亡、抗炎症、改善微循环方面概述其与肝脏缺血再灌注的关系。     

促红细胞生成素与心肌缺血再灌注损伤

近年来促红细胞生成素(erythropoietin,EPO)的非造血生物作用逐渐引起关注。研究表明,EPO 可以减轻缺血缺氧时心肌细胞的损伤,减少心肌细胞的调亡,从而使其可能成为预防和治疗心肌缺血再灌注损伤的一条途径。     

Toll样受体参与小鼠肝脏缺血再灌注损伤

目的探讨Toll样受体是否参与小鼠肝脏缺血再灌注损伤及其机制. 方法用Toll样受体缺损小鼠(C3H/Hej,Hej组)和野生型(C3H/Heouj,Heouj组)小鼠复制部分肝脏缺血再灌注损伤模型,于缺血45min,再灌注1h和3h处死动物,检测血清天门冬氨酸氨基转移酶(AST)和血清肿瘤坏死因子α(TNFα)的含量;并以northern blot及髓过氧化物酶(MPO)试验分别检测缺血肝组织TNFα mRNA的表达和MPO的含量. 结果 (1)再灌注1、3h,与假手术组相比,小鼠血浆AST明显升高,但Hej组明显低于Heouj组(661.83U/L±106.09U/L和1215.5U/L±174.03U/L,t＝-6.65,P<0.01;1145.17U/L±132.43U/L和2958.17U/L±186.81U/L,t＝-5.57,P<0.01);(2)再灌注3h时,与假手术组相比,Hej组和Heouj组小鼠血清TNFα浓度明显升高,且前者明显低于后者(152.39pg/ml±43.3pg/ml和249.12pg/ml±51.89pg/ml,t＝-3.13,P<0.05);(3)再灌注1h,除假手术组外,Hej组和Heouj组小鼠缺血肝组织内可见TNFα mRNA的表达,但前者的表达水平明显低于后者,杂交带密度分析显示两者之间差异有显著性 (80.3±28.8与189.4±24.6,t＝-3.25,P<0.05);(4)再灌注3h,与假手术组相比,Hej组和Heouj组小鼠缺血肝组织内MPO含量明显升高,且前者含量明显低于后者(0.059±0.004和0.173±0.025,F＝33.49,P<0.01). 结论 Toll样受体可能通过其介导的炎性通路参与了小鼠肝脏缺血再灌注损伤.