丹皮酚磺酸钠在动物肾缺血再灌注损伤中的作用

目的：了解丹皮酚磺的钠对肾缺血再灌注损伤模型肾组织病理改变及血浆丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性的影响。方法：将雄性新西兰大白兔右肾切除,阻断左肾动脉,制成肾缺血再灌注模型。按100mg/kg在不同时间应用丹皮酚磺酸钠进行干预治疗,比较不同时间血浆MDA含量和SOD活性变化以及术后48h肾组织病理变化。结果：应用丹皮酚磺酸钠治疗的大白兔。缺血再灌注60min时血浆MDA含量低于对照组,SOD活性高于对照组,肾脏病理改变减轻。结论：丹皮酚磺酸钠可以降低血浆MDA含量,增加SOD活性,对肾缺血再灌注损伤有保护作用。     

黄芪对肾缺血再灌注损伤的保护作用

目的 探讨黄芪注射液对肾脏缺血再灌注损伤的影响。方法 观察黄芪注射液对肾缺血再灌注损伤大鼠血浆超氧化物歧化酶（ＳＯＤ）,脂质过氧化产物丙二醇（ＭＤＡ）,内以素－１（ＥＴ－１）,一氧化氮（ＮＯ）变化及肾组织病理改变。结果 黄芪治疗组血浆ＥＴ０－１,ＭＤＡ水平较缺血再灌注组显著下降,ＳＯＤ显著升高,且病理改变较轻。结论 黄芪对肾脏缺血再灌注损伤具有保护作用。．     

缺血后处理对大鼠肾缺血再灌注损伤的影响

目的探讨缺血后处理对大鼠肾缺血再灌注损伤的影响。方法SD大鼠32只,雌雄不拘,随机分为4组（n=8）,假手术组（Ⅰ组）;对照组（Ⅱ组）建立肾缺血再灌注（I/R）模型;不同时间缺血后处理组（Ⅲ组和Ⅳ组）,建立I/R模型,Ⅲ组于缺血后再灌注10s,停灌10s,反复3次;Ⅳ组缺血后再灌注2min,停灌2min,反复3次。测定再灌注24h时血清尿素氮（BUN）、肌酐（Cr）浓度、超氧化物岐化酶（SOD）活性和丙二醛（MDA）浓度,光镜下进行肾组织病理形态学观察,采用免疫组化法测定肾组织血红素氧合酶-1（HO-1）表达。结果再灌注24h时,与Ⅰ组比较,其余3组血清Cr、BUN和MDA浓度升高,SOD活性和HO-1表达降低（P〈0.01）;与Ⅱ组比较,Ⅲ组和Ⅳ组血清Cr、BUN、MDA浓度和HO-1表达降低,SOD活性升高（P〈0.05或0.01）;Ⅲ组和Ⅳ组各指标差异无统计学意义（P〉0.05）。Ⅲ组和Ⅳ组病理改变明显轻于Ⅱ组。结论缺血后处理可减轻大鼠肾缺血再灌注损伤,其机制与上调HO-1的表达和清除氧自由基有关。     

缺血后处理对大鼠肾缺血再灌注损伤的影响

目的探讨缺血后处理对大鼠肾缺血再灌注（I／R）损伤的影响及其机制。方法18只雄性SD大鼠随机分为3组（n=6）：假手术组（S组）、缺血再灌注组（I／R组）和缺血后处理组（IPo组）。采用夹闭双侧肾蒂45min-再灌注6h制备肾脏缺血再灌注损伤模型。IPo组在夹闭双侧肾蒂45min后，再灌注10s，缺血10s，重复3次后，完全恢复肾血流。再灌注6h时开胸，取心脏血后处死大鼠，取肾组织。测定血清肌酐（Cr）、尿素氮（BUN）和尿酸（UA）浓度，肾组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性；光镜下观察肾组织病理学改变；采用原位末端脱氧核苷酸转移酶标记（TUNEL）法检测肾组织中凋亡细胞，光镜下计数凋亡细胞，并计算肾小管上皮细胞凋亡指数（AI）。结果与S组比较，I／R组和IPo组Cr和BUN浓度升高（P〈0．05），UA浓度差异无统计学意义（P〉0．05），肾组织SOD活性降低，MDA含量升高，肾小管上皮细胞凋亡指数增加（P〈0．05），病理损伤明显。与I／R组比较，IPo组Cr和BUN浓度降低（P〈0．05），UA浓度差异无统计学意义（P〉0．05），SOD活性升高，MDA含量降低，肾小管上皮细胞凋亡指数减少（P〈0．05），病理损伤减轻。结论缺血后处理能减轻大鼠肾缺血再灌注损伤，其机制与增强肾脏抗氧化能力和抑制肾组织细胞凋亡有关。     

缺血预处理对肾脏缺血再灌注损伤保护作用的研究进展

肾缺血再灌注损伤导致急性缺血性肾衰竭在临床上十分常见.研究显示缺血预处理对肾缺血再灌注损伤具有保护作用.近年来关于肾缺血预处理作用机制的报道较多,本文就缺血预处理对肾缺血再灌注损伤保护作用的研究现状作一综述.     

参芎注射液对肾缺血再灌注损伤大鼠的保护作用

目的观察参芎注射液对肾缺血再灌注损伤大鼠肾组织核因子-κB（NF-κB）、肿瘤坏死因子-α（TNF-α）、丙二醛（MDA）水平和超氧化物歧化酶（SOD）活性的影响,探讨其肾保护作用机制。方法将24只SD大鼠随机分为假手术对照组、缺血再灌注组、参芎预处理组,每组8只。免疫组织化学法检测各组大鼠肾组织NF-κB蛋白表达,酶联免疫吸附法检测肾组织TNF-α含量,用MDA和SOD试剂盒分别检测肾组织MDA含量和SOD活性。结果①与假手术对照组相比,缺血再灌注组大鼠肾组织NF-κB蛋白表达、TNF-α和MDA含量明显升高,差异均有统计学意义（P〈0．01）;而SOD的活性明显降低,差异有统计学意义（P〈0．01）。②与缺血再灌注组相比,参芎预处理组大鼠肾组织NF-κB蛋白表达、TNF-α和MDA含量降低,差异均有统计学意义（P〈0．05或P〈0．01）;而SOD的活性明显升高,差异有统计学意义（P〈0．01）。结论参芎注射液对肾缺血再灌注损伤有一定的保护作用,其机制可能与抗自由基氧化损伤以及抑制炎性细胞因子NF-κB和TNF-α的表达有关。     

黄芪甲甙对大鼠肾缺血再灌注损伤的保护作用

黄芪甲甙是黄芪单体之一 ,除了有抗炎 ,降压 ,改善心肌缺血等作用外 ,还具有抗脂质过氧化及清除自由基作用 ,我们观察了黄芪甲甙对大鼠肾缺血再灌注损伤的影响。一、材料与方法1.试剂与仪器 :黄芪甲甙 (纯度为83 .73 % ,上海药品检验所 ) ,实验前用生理盐水 (NS)配制成 1%、5 %和 10 % (g/L)溶液 ;超氧化物歧化酶 (SOD)试剂盒由南京建成生物研究所提供。大鼠肿瘤坏死因子 (TNF ) α酶联免疫吸附法(ELISA)试剂盒购自晶美公司。仪器 :酶标仪 (BioTEKELX80 0 ) ,分光光度计(PharmaciaBiotechUltrospect 2 0 0 0 )。2 .动物分组及方…     

褪黑素对急性肾缺血再灌注损伤的预防作用

褪黑素 (Ｍｅｌ)是松果体合成分泌的神经内分泌激素 ,有多种生物学功能。近十年的研究证实它是迄今已知的最强的自由基清除剂 ,国内尚未见相关的研究报道。我们用钳夹大鼠双侧肾蒂造成急性肾缺血再灌注损伤 (ＡＲＩＩ)动物模型 ,探讨褪黑素对ＡＲＩＩ的预防保护作用。一、材料与方法1.动物分组与模型 :36只健康成年ＳＤ大鼠 ,雄性 ,随机分为 6组 (ｎ =6 ) :(1)假手术对照组 ;(2 )手术对照组 :缺血前 30分钟腹腔注射生理盐水 0 3ｍｌ作为阴性对照 ;(3)手术 维生素Ｃ组 :按15 0ｍｇ/ｋｇ计算 ,于缺血前 30分钟腹腔注射作为阳性对照 ;(4)～ (…     

新型铁螯合剂CHGN2957对大鼠肾缺血再灌注损伤的保护作用

目的 观察新型铁螯合剂CHGN2957对大鼠肾缺血再灌注损伤(I/R)急性期的保护作用.方法 选用雄性SD大鼠90只,随机分成5组(n=18):假手术组、CHGN2957高剂量组、低剂量组、溶剂组和阳性对照组.建成大鼠急性肾I/R模型.药物干预均从手术前2 d开始,直至术后12 d结束.观察大鼠死亡率、体质量变化,测定肾功能和肾组织中超氧化物歧化酶(SOD)活力、谷胱甘肽(GSH)还原酶活力和丙二醛(MDA)含量并进行肾组织病理切片观察.结果 术后第3天CHGN2957溶剂组的体质量(242.1±16.2)g、SOD活力(1.23±0.13)U/mg、GSH还原酶活力(336±15)U/L明显低于其他各组(P＜0.05),而血清尿素氮(62.3±3.1)mmol/L、血清肌酐(310.00±21.02)μmol/L、MDA含量(186.5±16.7)nmol/mg明显高于其他各组(P＜0.05).肾组织病理评分显示CHGN2957溶剂组的肾小管损伤明显重于其他各组(P＜0.05).结论 CHGN2957作为一种新型铁螯合剂,在大鼠急性肾I/R过程中能有效减轻大鼠肾I/R,并对肾起保护作用.

Abstract：

Objective To observe the protecgive effects of CHGN2957 on acute renal ischemia/reperfusion injury (I/R) model in rats. Methods Ninety Sprague-Dawley male rats were randomly divided into five groups ( n = 18 each): sham-operative group, high-dose CHGN2957 group, low-dose CHGN2957 group, CHGN2957 vehicle group and positive group. The administration lasted from two days before operation to twelve days after operation. After seccessful establishment of the model, mortality,weight changes, the renal function, superoxide dismutase ( SOD ) activity, glutathione ( GSH ) reductases activity and malondialdehyde (MDA) content in renal tissue were recorded, and the pathological changes were observed. Results Weight (242. 1 ± 16. 2) g, SOD activity (1. 23 ±0. 13) U/mg and GSH reductases activity (336 ± 15 U/L) in CHGN2957 vehicle group were reduced significantly as compared with other groups three days after I/R (P ＜0. 05), but SUN (62. 3 ± 3. 1) mmol/L, SCr (310. 00 ± 21. 02)μmol/L, MDA content ( 186. 5 ± 16. 7 ) nmol/mg were higher than others obviously ( P ＜ 0. 05 ). Pathological observation showed renal tubular injury was more serious in CHGN2957 vehicle group (P＜0.05).Conclusion CHGN2957 as a new iron chelator was effective to ameliorate renal I/R in rats.     

川芎嗪在大鼠肾脏缺血再灌注损伤中的作用

目的：探讨川芎嗪对大鼠肾脏缺血再灌注损伤的保护作用。方法：观察川芎嗪注射液对大鼠肾脏缺血再灌注损伤后血浆超氧化物歧化酶（SOD）、脂质过氧化物丙二醇（MDA）、内皮素－1（ET－1）的作用及肾小管损伤形态学的影响。结果：川芎嗪治疗组大鼠血浆SOD水平较缺血再灌注组显著升高（P＜0.05)，MDA和ET－1水平显著性下降（P＜0.05)，肾小管损伤的病理分级显著减轻（P＜0.05)。结论：川芎嗪对肾脏缺血再灌注性损伤具有保护作用。     

葡天胶囊对大鼠肾脏缺血再灌注损伤的保护作用

目的：探讨葡天胶囊预处理对大鼠肾脏缺血再灌注损伤的保护作用。方法：雄性Wistar大鼠24只,随机分为假手术组（Sham组）、模型对照组（Control组）、葡天胶囊预处理组（PT组）,每组各8只。模型对照组及葡天胶囊160mg·kg^-1·d^-1预处理组手术建立肾脏缺血再灌注模型,缺血后1h恢复灌注,分别在恢复灌注后24h、48h、72h后检测血肌酐、尿素氮及血清白蛋白水平,并观察肾脏病理变化。结果：与假手术组相比,模型组血肌酐水平升高（P〈0.05）;葡天胶囊预处理组再灌24h、48h及72h血肌酐水平明显低于模型组（P〈0.05）;肾脏病理显示葡天胶囊预处理组肾组织病变轻于模型对照组。结论：葡天胶囊对肾脏缺血再灌注损伤有保护作用,具有一定的临床应用价值。     

己酮可可碱在肺缺血-再灌注损伤中的作用

目的　探讨己酮可可碱 (PTX)对肺缺血 -再灌注损伤的保护作用。　方法　 72只大鼠随机分为 3组 ,每组 2 4只。 组 :未行缺血及再灌注处理 ; 组 :行左肺缺血和再灌注处理 ; 组 :行左肺缺血和再灌注处理 ,并给予己酮可可碱。采用在体肺温缺血 -再灌注损伤的模型 ,于缺血 45分钟、再灌注 1小时、2小时和 4小时进行动脉血气分析、肺组织含水量、支气管肺泡灌洗液白蛋白含量、血浆和左肺组织丙二醛、左肺组织和支气管肺泡灌洗液髓过氧化物酶(MPO)活性测定。　结果　 组再灌注 2小时和 4小时动脉血氧分压显著降低 ,各时间点左肺含水量、支气管肺泡灌洗液白蛋白含量、血浆丙二醛、左肺组织、支气管肺泡灌洗液中髓过氧化物酶均显著升高 ,PTX可改善上述指标变化。结论　 PTX通过抑制中性粒细胞肺内聚集 ,减轻肺血管内皮细胞损伤程度 ,而防止损伤的发展     

人参皂甙Rb1对肺缺血再灌注损伤的保护作用

目的探讨人参皂甙Ｒｂ１对肺缺血再灌注损伤的保护作用。方法按肺移植供肺获取和保存的方法，对３５只家兔的肺分别获取，保存；然后采用体外装置，建立体外肺缺血再灌注损伤模型。在即将再灌流前，将不同剂量的Ｒｂ１加入到５０ｍｌ再灌流血液中。结果Ｒｂ１可使肺组织中超氧化物歧化酶（ＳＯＤ）含量升高，丙二醛（ＭＤＡ）含量降低；使肺动脉压（ＰＡＰ）降低，湿肺干肺比重降低和改善肺组织病理变化。Ｒｂ１在再灌流血液中浓度为８０ｍｇ／Ｌ时，已有明显效果。结论Ｒｂ１对肺缺血再灌注损伤具有明显的保护作用。     

Effects of Intravenous Anesthetics on Renal Ischemia/Reperfusion Injury

Background. Renal ischemia/reperfusion (I/R)-induced tubular epithelial cell injury, called ischemic acute renal failure, is associated with high mortality in humans. Protecting the kidney against I/R injury is very important during complicated renal operations, transplantation surgery, and anesthesia. Aim. The purpose of this study was to investigate and compare the efficiency of ketamine, thiopental, propofol, etomidate, and intralipid in reducing the injury induced by free radicals in a rat model of renal I/R. Method. Forty-two Wistar rats were divided into seven groups in our study. Rats in the sham group underwent laparotomy and waited for 120 minutes (min) without ischemia. Rats in the control group were given nothing with ischemia-reperfusion. Rats in the I/R groups were given ketamine (20 mg/kg), thiopental (20 mg/kg) propofol (25 mg/kg), etomidate (10 mg/kg) and 10% intralipid (250 mg/kg) intraperitoneally 15 min prior to the ischemia for 60 min, followed by reperfusion for 60 min. The blood samples and kidney tissues of the rats were obtained under anesthesia at the end of the reperfusion period. Biochemical malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), blood urea nitrogen (BUN), creatine (Cr), aspartate aminotransferase (AST) were determined, and histopathological analysis was performed with these samples. Results. MDA level was increased significantly in the control group (p < 0.05). Histopathological findings of the control group confirmed that there was renal impairment by tubular cell swelling, interstitial edema, medullary congestion, and tubular dilatation. MDA levels were lower in the ketamine, thiopental, and propofol groups compared to the control group (p < 0.05). In the thiopental and propofol groups, the levels of histopathological scores were significantly lower than control and etomidate groups in ischemia-reperfusion. Conclusion. Our results demonstrated that I/R injury was significantly reduced in the presence of propofol and thiopental. The protective effects of these drugs may belong to their antioxidant properties. These results may indicate that propofol and thiopental anesthesia protects against functional, biochemical, and morphological damage better than control in renal I/R injury.     

新霉素对脑缺血再灌注损伤的保护作用

目的：探讨钙及磷酯酶Ｃ（ＰＬＣ）在脑缺血再灌注损伤中的作用机制及ＰＬＣ抑制剂新霉素是否通过抑制ＰＬＣ活性而起脑保护作用。方法：和放血降压法建立大鼠全脑缺血模型，采用原子吸收光谱法及干湿法测定缺血再灌注后脑组织含钙量。含水量变化及新霉素对其影响。结果：再灌组含钙量、含水量较对照组升高（Ｐ〈０．０５）；再灌组内随灌注时间延长，脑组织含钙量、含水量增高（Ｐ〈０．０５）；给药组含钙量、含水量均较再灌组降低     

超前缺血对培养乳鼠心肌细胞缺血再灌注损伤保护作用的实验研究

观察超前缺血（ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇｗｉｔｈｉｓｃｈｅｍｉａ，ＰＣＩ）对培养乳鼠心肌细胞缺血再灌注（ｉｓｃｈｅｍｉａ－ｒｅｐｅｒｆｕｓｉｏｎ，Ｉ－Ｒ）损伤的影响。发现（１）心肌细胞经ＰＣＩ后，其ＡＴＰ含量及培养液ＬＤＨ无明显变化；（２）经ＰＣＩ诱导的心肌细胞，持续３ｈ缺糖、缺氧，其ＡＴＰ消耗较对照组显著减少；（３）复灌期ＰＣＩ组ＡＴＰ含量增加，ＬＤＨ下降；（４）在各时相［Ｃａ＋＋］ｉ与对照组比较无明显变化，但ＬＰＯ于复糖、复氧后显著降低。结果提示：有限次数短暂ＰＣＩ对心肌细胞代谢及膜通透性无损伤作用；ＰＣＩ能提高细胞对长时间缺氧的耐受能力，减轻缺氧心肌Ｉ－Ｒ损伤。其机理可能是：心肌细胞作为一独立的基本功能单位，经ＰＣＩ诱导，细胞内抗氧自由基系统酶的活性增加，减轻了氧自由基的损伤效应。     

Oxidized LDL Accumulation in Experimental Renal Ischemia Reperfusion Injury Model

Background/Aims. The aim of this study was to identify oxidative damage of kidney during ischemia reperfusion injury (IRI) by evaluating changes in lipid peroxidation markers in tissue and blood by an experimental model. Oxidized LDL (ox-LDL) was used as an oxidative stress biomarker, whereas paraoxonase (PON-1) activity was used as an antioxidative biomarker. Methods. Sixty-three male Wistar rats were randomly assigned into three groups: renal IRI, sham, and control. In the renal IRI group, the right kidney was removed and the artery and vein of the left kidney were clamped for 90 minutes. The presence of ox-LDL in the kidney tissue sections was determined by using an immunofluorescent staining method. Results. The plasma ox-LDL levels did not increase significantly at the 24^th hour following IRI, made a peak at the 48^th hour, and declined at the 72^nd hour. Accumulation of ox-LDL was detected in the kidney tissue on the 24^th, 48^th, and 72^nd hours of the renal IRI. Serum PON-1 levels have peaked on the 24^th hour and then declined. Conclusion. This study demonstrates the accumulation of ox-LDL molecules in the renal tissues of the IRI model. Future strategies aimed to reduce the lipid peroxidation during the initial hours of renal IRI may be useful to prevent complications of ischemia.     

细胞外高钾对离体鼠心缺血再灌注损伤的保护作用

为了解高钾抗心肌缺血再灌注（Ｉ－Ｒ）损伤的途径。用离体大鼠心脏行冠脉结扎，松扎后作电镜观察和磷酸盐－焦锑酸盐（ＰＰＡ法）细胞化学钙定位及抗氧自由基检测。结果：１３ｍｍｏｌ／Ｌ高钾保护Ｉ－Ｒ心肌超氧化物歧化酶（ＳＯＤ）活力，抑制丙二醛（ＭＤＡ）生成，减少心肌酶的漏出，保存肌膜结合钙的能力，防止钙在线粒体的积聚，减轻心肌超微结构的破坏。实验提示１３ｍｍｏｌ／Ｌ钾能抑制胞内钙超负荷和膜脂质过氧化达到抗Ｉ     

Ameliorative Effects of Proanthocyanidin on Renal Ischemia/Reperfusion Injury

Introduction. Several natural products have been reported to have beneficial effects on ischemia/reperfusion (I/R) injury, particularly from a preventative perspective. Therefore, this study was designed to investigate the efficiency of proanthocyanidin (PA), a natural product derived from grape seed, on renal dysfunction and injury induced by I/R of rat kidney. Materials and Methods. Twenty-four male Sprague-Dawley rats were divided into three groups: sham-operated, I/R, I/R+PA. Rats were given PA (100 mg/kg/day peroral) 7 days prior to I/R. All rats except sham-operated underwent 60 min of bilateral renal ischemia followed by 6 h of reperfusion. After reperfusion, kidneys and blood were obtained for evaluation. Superoxide dismutase, glutathione peroxidase, malondialdehyde, protein carbonyl content, and nitrite/nitrate level (NO_x) were determined in the renal tissue. Serum creatinine (S_Cr), blood urea nitrogen (BUN), and aspartate aminotransferase (AST) were determined in the blood. Additionally, renal sections were used for histological grade of renal injury. Results. PA significantly reduced the I/R-induced increases in S_Cr, BUN, and AST. In addition, PA markedly reduced elevated oxidative stress product, restored decreased antioxidant enzymes, and attenuated histological alterations. Moreover, PA attenuated the tissue NO_x, levels indicating reduced NO production. Conclusions. The pretreatment of rats with PA reduced the renal dysfunction and morphological changes, ameliorated cellular injury, and restored renal antioxidant enzymes caused by renal I/R.