黄芪对幼兔缺血再灌注后肠黏膜细胞凋亡的影响及对肠黏膜屏障的保护

目的 研究黄芪对幼兔肠缺血再灌注后肠黏膜细胞凋亡的影响及肠黏膜屏障的保护作用.方法 雄性幼兔20只,分假手术组、肠缺血再灌注组(模型组)、黄芪组、生理盐水组(对照组);黄芪组在手术前7天予黄芪腹腔注射6 mg/(kg·d),对照组每天予等量生理盐水.在手术时制作肠缺血再灌注模型,观察小肠组织及血浆超氧化物歧化酶(SOD)活性、肠黏膜细胞凋亡指数、肠黏膜形态损伤情况及黄芪对其改变的影响.结果 肠缺血再灌注后血浆及小肠组织SOD活性明显降低,肠黏膜细胞凋亡指数明显增加,小肠黏膜形态及肠黏膜屏障功能损害加重,黄芪能显著改善上述改变.结论 黄芪对幼兔肠缺血再灌注肠黏膜屏障损伤有明显的保护作用.     

双氯灭痛对小肠缺血,再灌注损伤细胞保护作用的实验研究

目的：观察双氯灭痛对大鼠小肠缺血，再灌注损伤的细胞保护作用，方法：口饲双氯灭痛１２．５ｍｇ／只后，阻断肠系膜上动脉，造成大鼠肠缺血，再灌注模型２０只，光镜观察肠损伤程度。结果：缺血，再灌注对肠壁组织可造成损伤，口饲双氯灭痛组与对照组相比肠壁损伤明显减轻（Ｐ〈０．０５），结论：双氯灭痛对大鼠小肠缺血，再灌注损伤有保护作用。     

新生猪仔肠缺血再灌注所致细菌移位的实验研究

目的 了解新生儿肠缺血再灌注损伤对细菌移位的影响。方法 采用新生猪仔非阻塞性肠缺血再灌注模型,观察不同程度缺血再灌注所致肠道细菌移位及肠粘膜上皮损伤情况。结果 对照组无细菌移位,中度缺血仅有肠系膜淋巴结细移位移,中度缺血再灌注,重度缺血,重度缺血再灌注均导致肠系膜淋巴结,外周血,肝,脾细菌移位,缺血再灌注组细菌移痊数明显高于仅有缺血组（Ｐ〈０．０１）,重度缺血再灌注可见肠粘膜上皮损伤。结论 新生猪     

雌激素对青春期雌性大鼠肠缺血再灌注损伤的保护作用

目的：探讨雌激素对肠缺血再灌注损伤的影响。方法：取雌性青春期大鼠，分为卵巢切除组（20只）、对照组（10只）、雌二醇组（10只），大剂量雌二醇组（20只）。观察肠缺血30min再灌注60min后肠粘膜损伤程度(Chiu氏评分法），测定血清雌二醇，NO2^－／NO3^-和丙二醛水平。结果：雌二醇组和大剂量雌二醇组的Chiu氏评分法和丙二醛低于卵巢切除组，而NO2^-／NO3^－高于卵巢切除组。雌二醇Chiu氏评分法呈负相关，与NO2^-／NO3^3－呈正相关，结论：雌激素对青春期雌性大鼠肠缺血再灌注损伤有一定的保护作用。     

肠脂肪酸结合蛋白(Ⅰ-FABP)在肠缺血早期诊断的意义

目的本试验对肠脂肪酸结合蛋白和各种生物学指标进行比较,决定其用于早期诊断肠缺血的可行性.方法用成年健康SD大鼠20只,分为实验组Ⅰ(n=10)和对照组Ⅱ(n=10),各组10只,体重250～300g.每只SD大鼠肌注10%水合氯醛5mg/kg麻醉.对照组仅无菌条件下打开腹腔;实验组沿腹中线打开腹腔,将肠系膜上动脉根部游离,用无创动脉夹夹闭60min后,放开无创动脉夹再灌注60min.分别于术前、术后15、30、60min和去除无创动脉夹后30、60min采集静脉血.同时肠组织光镜下评分.结果肠脂肪酸结合蛋白肠缺血15min时可达到对照组的十数倍,缺血30min时可达高峰,再灌注损伤30min后下降,但还是为对照组血清浓度的数百倍,两组存在着显著差异(P＜0.001).血清CK实验组缺血30mim达高峰,约为对照组的3～4倍.血清COT实验组随时间逐渐增加,缺血60min时达高峰,再灌注时逐渐下降.各时期与对照组比较无显著差异.血清LDH在缺血60min内两组有区别(P＜0.05).实验组和对照组在缺血60min以内,两组肠黏膜损伤程度无明显差异,再灌注损伤发生后两组出现差异(P＜0.05).结论肠脂肪酸结合蛋白可以作为早期肠缺血较理想的生物学指标.     

大鼠肠缺血再灌注后肠粘膜细胞凋亡和内源性一氧化氮的观察

临床上一直缺少对肠缺血再灌注损伤的检测指标。本实验通过对肠道缺血前后及再灌注后血清一氧化氮浓度的测定 ,肠粘膜细胞的凋亡等改变 ,以期探讨损伤后血清一氧化氮浓度及粘膜细胞凋亡的变化规律 ,指导临床工作。1 .动物模型的制作　ＳＤ成年雄性大鼠 1 2只 ,体重 (2 75± 50 )ｇ ,以腹腔注射 1 %戊巴比妥钠 30～ 50ｍｇ/ｋｇ麻醉 ,消毒 ,置气管插管维持呼吸道通畅 ,置颈内动脉插管以取血用。正常组仅做开腹及关腹手术为对照。实验组开腹 ,钳夹肠系膜上动脉 60ｍｉｎ后 ,解除钳夹再灌注 2ｈ制成小肠缺血再灌注的动物模型。2 .实验分组　正…     

肠脂肪酸结合蛋白（I—FABP）在肠缺血早期诊断的意义

目的　本试验对肠脂肪酸结合蛋白和各种生物学指标进行比较 ,决定其用于早期诊断肠缺血的可行性。方法　用成年健康SD大鼠 2 0只 ,分为实验组Ⅰ (n =10 )和对照组Ⅱ (n =10 ) ,各组 10只 ,体重 2 5 0～ 30 0g。每只SD大鼠肌注 10 %水合氯醛 5mg/kg麻醉。对照组仅无菌条件下打开腹腔 ;实验组沿腹中线打开腹腔 ,将肠系膜上动脉根部游离 ,用无创动脉夹夹闭 6 0min后 ,放开无创动脉夹再灌注 6 0min。分别于术前、术后 15、30、6 0min和去除无创动脉夹后 30、6 0min采集静脉血。同时肠组织光镜下评分。结果　肠脂肪酸结合蛋白肠缺血 15min时可达到对照组的十数倍 ,缺血 30min时可达高峰 ,再灌注损伤 30min后下降 ,但还是为对照组血清浓度的数百倍 ,两组存在着显著差异 (P <0 .0 0 1)。血清CK :实验组缺血 30min达高峰 ,约为对照组的 3～ 4倍。血清GOT :实验组随时间逐渐增加 ,缺血 6 0min时达高峰 ,再灌注时逐渐下降。各时期与对照组比较无显著差异。血清LDH :在缺血 6 0min内两组有区别 (P <0 .0 5 )。实验组和对照组在缺血 6 0min以内 ,两组肠黏膜损伤程度无明显差异 ,再灌注损伤发生后两组出现差异 (P <0 .0 5 )。结论　肠脂肪酸结合蛋白可以作为早期肠缺血较理想的生物学指标。     

红花对兔肠缺血再灌注损伤时血白细胞介素8和肠超微结构变化的影响

目的 探讨红花对兔肠缺血再灌注损伤时血白细胞介素8和肠组织超微结构变化的影响及机制.方法 复制在体兔肠缺血再灌注损伤模型.30只日本大耳兔,随机均分为三组:假手术组(S组),缺血再灌注组(IR组)和缺血再灌注+红花注射液组(SI组).分别于缺血前,再灌注0、1、2、3h检测兔血清白细胞介素8的浓度,及电镜下观察肠组织形态学改变.结果 IR组血清白细胞介素8水平随缺血和再灌注时间的延长而逐渐升高,缺血和再灌注各时点均明显高于S组(P<0.01);SI组稍有上升变化,且明显低于IR组上升程度,肠组织超微结构异常改变不同程度减轻.结论 红花在兔肠缺血再灌注损伤中能有效地抑制血白细胞介素8的合成和释放,对肠组织超微结构有良好保护作用.     

肠缺血再灌注时肿瘤坏死因子免疫组织化学研究

目的　探讨肠缺血 /再灌注时肿瘤坏死因子 (tumornecrosisfactorα,TNF α)的来源及作用。方法　① 4 8只雄性Wistar大白鼠体重 (130± 15 ) g ,分成 6组 (n =8) ,假手术组 ,缺血 30min组 ;缺血 30min ,再灌注组 ;缺血 30min ,再灌注 6 0min组 ;缺血 30min ,再灌注 90min组 ;缺血 12 0min组 ;②利用免疫组织化学技术检测肠、肝组织TNF α蛋白表达和分布。③对肠组织进行HE染色。结果　①肠粘膜免疫组化于缺血 130组 ;缺血 30min ,再灌注 6 0min组 ;缺血 30min ,再灌注 90min组时可见TNF α强阳性物质 ,缺血 30min ,再灌注 90min组 ;可见极强阳性物质 ;②缺血 30min ,再灌注 30min组 ;缺血 30min ,再灌注 6 0min组肝组织内可见阳性物质 ,缺血 30min ,再灌注 90min组 ;为强阳性物质 ;③肠组织HE染色显示I30’G肠粘膜轻度受损 ,缺血 30min ,用灌注 30min组 ;缺血 30min ,再灌注 6 0min组 ;缺血 30min ,再灌注 90min组肠粘膜中度受损 ,再灌注 12 0min组肠粘膜重度受损。结论　幼鼠肠缺血 /再灌注后TNF α在肠、肝内均有阳性反应 ,但肠粘膜内TNF α较肝内明显 ,因此推论幼鼠肠缺血 /再灌注损伤早期TNF α可能主要来源于肠组织 ,并且介导幼鼠肠缺血 /再灌注损伤的病理过程     

液体呼吸剂治疗大鼠肠缺血再灌注损伤的实验研究

目的　探讨含氧液体呼吸剂灌注对大鼠肠缺血再灌注损伤的治疗作用。方法　SD成年雄性大鼠 2 7只 ,随机分为IIR组 (7只 )、含氧生理盐水 (NS O2 )组 (7只 )、液体呼吸剂 (PFC)组 (6只 )及含氧液体呼吸剂 (PFC O2 )组 (7只 ) ,在肠缺血期分别灌注肠腔 ,测定各组缺血前后和再灌注后 2h血清NO、内皮素 (ER)、肠组织匀浆MDA含量 ;观察肠粘膜病理变化、粘膜TUNEL染色阳性细胞数和caspase 3平均灰度值。 结果　PFC O2 组肠粘膜病理改变显著减轻 ,病变局限于肠粘膜表层 ;MDA含量也较IIR组、NS O2 组和PFC组显著减少 (P <0 .0 1)。含氧PFC灌注血清NO浓度明显升高 (P <0 .0 1) ,ET浓度明显下降。肠粘膜中TUNEL染色阳性细胞数和caspase 3组化染色阳性率显著低于对照组。血清NO浓度与TUNEL阳性细胞数相关回归分析呈显著负相关 (y =- 1.77x 14 0 .8,r =0 .97,P <0 .0 5 )。结论　含氧PFC灌注对肠IIR损伤起保护作用 ,其作用机制可能与改善氧供、减少氧自由基生成、提高NO浓度、下调ET浓度和抑制细胞凋亡有关。     

白藜芦醇对大鼠肠缺血再灌注损伤的保护作用

目的 探讨白藜芦醇(resveratro1,RES)对实验性大鼠肠缺血再灌注肠黏膜损伤的保护作用.方法 24只成年雄性SD大鼠随机分为假手术组(SO)、缺血再灌注损伤组(I/R)、RES治疗组.SO组仅分离肠系膜上动脉(SMA)根部而不夹闭.肠缺血再灌注损伤组(I/R)和RES治疗组均用无损伤血管夹夹闭SMA根部后分别立即经阴茎背静脉注射生理盐水、RES(20 mg/kg),45 min之后放松血管夹形成再灌注.各组大鼠均于制模后6 h采集标本.检测血清和回肠组织中的超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,TUNEL法检测肠黏膜上皮细胞凋亡率,并观察肠黏膜病理变化.结果 小肠缺血再灌注后,血清及小肠组织中反映氧化损伤程度的MDA明显升高,SOD则明显减少,小肠黏膜上皮细胞凋亡,应用RES后能显著改善上述改变.结论 白藜芦醇对肠缺血再灌注损伤具有保护作用,其机制可能与通过抗氧化作用及抑制肠黏膜上皮细胞凋亡有关.

Abstract：

Objective To study the protective effects of resveratrol (RES) on intestinal ischemia-reperfusion injury in rats.Methods Twenty-four SD rats were randomly divided into the sham operation group,intestinal ischemia-reperfusion injury (I/R) group and resveratrol treated (RES) group.The intestinal ischemia injury was induced by superior mesenteric artery occlusion for 45 minutes,and then the blood supply to the intestine was restored to cause reperfusion injury.After 6 hours' reperfusion,the rats were sacrificed and intestine was collected.Of the RES group,the rats were subjected to I/R injury,and treated with 20 mg/kg resveratrol by intravenous injection immediately after the mesenteric artery was clamped.Superoxide Dismutase (SOD) and Malonaldehyde (MDA) levels in serum and intestine were measured.Apoptotic intestinal epithelial cells were detected by TUNEL methods.The histological injury of the intestine was also examined.Results Compared with the sham operated rats,MDA levels in the serum and intestine as well as the apoptotic epithelial cells were significantly increased in the rats subjected to I/R (MDA in serum and intestine 4.63±0.53 vs 1.32±0.40;8.60± 0.98 vs 4.13±0.86,P＜0.01;apoptotic index 66.63 ± 1.71 vs 46.72 ± 1.50,P＜0.01 ).However,the SOD levels in the serum and intestine were decreased (49.21±4.38 vs 86.65±6.14;351.03 ± 21.46 vs 468.93 ± 16.21,P＜0.01).In the rats subjected to I/R injury but received resveratrol treatment,the epithelial cells apoptosis and MDA levels in serum and intestine were decreased,and SOD levels in serum and intestine increased (P＜0.05).Conclusions Resveratrol protects intestine from ischemia-reperfusion injury in rats.     

内皮素1受体拮抗剂对大鼠小肠缺血再灌注肺损伤的作用研究

目的 探讨内皮素—1受体拮抗剂BQ—610对大鼠小肠缺血再灌注过程中的抗肺损伤作用及可能的机制。方法 SD大鼠分为3组，第1组为对照组，第2组为缺血再灌注组，第3组为缺血再灌注后使用BQ—610组。比较3组阻断肠系膜上动脉血流80min，开放再灌注120min后肺组织的受损情况。结果 小肠缺血再灌注后肺组织内皮素升高，降钙素基因相关肽下降，肺组织内出血、大量白细胞聚集，髓过氧化物酶活性增加；应用BQ—610后，内皮素变化不显著，降钙素基因相关肽下降，肺组织内出血、白细胞聚集减少，髓过氧化物酶活性也下降。结论 BQ—610不但可以阻断内皮素1受体，还能调节肺组织内内皮素、降钙素基因相关肽变化，并对小肠缺血再灌注所致的肺损伤有一定的保护作用。     

Reduced apoptosis in newborn compared to adult rat intestine after ischemia-reperfusion injury

The pathogenesis of necrotizing enterocolitis (NEC) is unknown. Ischemia and reperfusion (I/R) injury has been considered to be a major contributing factor. More recent reports have noted that apoptosis is a significant and perhaps the principal contributor to cell death after I/R. Some reports revealed that infants with NEC and perforated bowel can completely recover with drainage alone. This study aims to assess the ability of newborn rat intestine to resist apoptosis after I/R injury compared with adult rat intestine. Intestines from 10 groups of rats (n = 6 for each study group) were studied: (1) normal control group; (2) ischemia group, receiving vascular occlusion for 60 min; (3) I/R groups receiving vascular occlusion for 60 min and reperfusion for 15, 30, and 60 min, respectively. Apoptosis was quantified by TUNEL methods. Statistical analysis was performed using ANOVA with Dunn's test. TUNEL-positive cells per 10 crypts were significantly increased in the ischemia and I/R groups compared to the control group. The peak number of positive cells by TUNEL was recognized 30 min after reperfusion in adult and newborn rats and then reduced gradually. The newborn rats had significantly less TUNEL-positive cells per 10 crypts than adult rats subjected to I/R injury (p < 0.05). We demonstrated that the activation of apoptosis occurred after intestinal I/R injury, especially during the reperfusion phase. The newborn intestine was more resistant to I/R injury and thus may have significant clinical application.     

甲泼尼龙对幼鼠心肌缺血再灌注损伤免疫反应的抑制作用

目的 探讨甲泼尼龙对幼年大鼠心肌缺血再灌注损伤(MIRI)血清IL-1、8、10水平的影响,探讨其对心肌的保护作用.方法 70只健康清洁级2～4周龄大鼠随机分为3组:对照组10只,模型和药物组各30只.后二组又分为缺血0.5 h,再灌注2、4、8、12、24 h共6个亚组(各5只),对照组只取12 h一个时相点作总体对照.建立MIRI模型,比较各组心肌形态学变化,检测其血清IL-1、8、10的动态表达.采用SPSS 10.0软件进行统计学分析.结果 光镜下,对照组心肌细胞无变化;模型组有炎性细胞浸润及心肌细胞变化坏死,并随再灌注时段的延长而加重;药物组各时段炎性反应及心肌细胞变性坏死程度均明显轻于模型组.模型与药物组比较心肌炎性反应明显减弱,同一时相点IL-1、8的表达显著降低(Pa＜0.05),IL-10表达升高且峰值提前至缺血再灌注8 h.结论 适当应用甲泼尼龙可通过抑制IL-1、8及促进IL-10的分泌而起到保护缺血心肌的作用.     

Serum cytosolic beta-glucosidase activity in a rat model of necrotizing enterocolitis

The diagnosis of necrotizing enterocolitis (NEC) is made from a combination of clinical and radiographic findings. There are no useful screening biochemical markers of intestinal injury. The serum concentration of cytosolic beta-glucosidase (CBG), an enzyme found primarily in enterocytes, is markedly elevated in animal models of ischemia and bowel obstruction. We hypothesized that in a rat model of NEC, serum CBG activity would significantly increase before microscopic evidence of severe intestinal injury. Cohorts of 2-wk-old Sprague-Dawley rats (n = 10/cohort) were anesthetized and underwent laparotomy with occlusion of the superior mesenteric artery (SMA). Platelet-activating factor (200 microg/animal) was injected in the proximal duodenum. Serum and intestinal samples were obtained at time 0 (control) and 30, 60, and 90 min of ischemia (I) and after 90 min of I followed by 60 min of reperfusion (I/R). Histopathologic injury was categorized as either no or minimal injury or mural necrosis by two masked investigators and CBG activity was measured by ELISA. Data were analyzed with Fisher's exact test and ANOVA. Only the I/R group had significantly greater mural necrosis compared with the control group (90% versus 0%, respectively, p < 0.001). In contrast, CBG activity was significantly elevated after only 90 min of I and after I/R (15.1 +/- 5.6 and 16.4 +/- 4.3 units/mL, respectively, p < 0.05). We conclude that serum CBG is elevated before transmural intestinal injury in this model and may have utility as an early marker of ischemia in patients at risk for NEC.     

雌激素对大鼠肠缺血再灌注损伤的保护作用及对iNOS表达的影响

目的探讨雌激素对肠缺血再灌注损伤（I／R）的保护作用及对诱导型一氧化氮合酶（i—NOS）表达的影响。方法将60只青春期大鼠随机分为4组（每组各15例），假手术组未切除卵巢，其余3组行双侧卵巢切除术，术后隔天分别皮下注射蓖麻油（对照组）、雌二醇（E2，100ug／kg，E2组）、高剂量的E2（500ug／kg，5E2组）4周。将各组大鼠肠系膜上动脉夹闭30min，再灌注时间分别为1h（n=5）、6h（n=5）和24h（n=5）。测血清E：浓度，小肠粘膜行粘膜病理评分、iNOSmRNA表达及iNOS活性测定。结果对照组、假手术组、E2组和5E2组小肠粘膜病理评分分别为3．31±0.12、3.00±0．09、2.57±0．12和2．98±0．08，iNOSmRNA表达水平的拷贝数对数值分别为3.85±0.42、4.86±0.76、5．17±0．34和4．25±0．41。E2组的病理评分低于其它3组（P〈0．01），而iNOSmRNA表达水平高于其它3组（P〈0.01）。各组iNOS活性水平与iNOSmRNA表达水平一致，E2组iNOS活性高于对照组（P〈0．05），亦高于假手术组和5E2组（P值均〈0．05）。线性回归分析示血清E2浓度的对数值与病理评分呈负相关（P〈0.01）、与iNOSmRNA和iNOS活性呈正相关俨值均〈0.01）。结论雌激素对大鼠肠I／R损伤有保护作用，该保护作用与iNOS表达增强有关。     

Pentoxifylline attenuates ischemia/reperfusion injury to the small intestine in the rat

There is a large body of evidence that neutrophils may play an important role in the mucosal injury that follows ischemia of the intestine. Pentoxifylline (PTF), a methylxanthine derivative, prevents leukocyte adherence to vascular endothelium and restores intestinal blood flow following hemorrhagic shock and sepsis. The purpose of this study was to evaluate the protective properties of PTF in an ischemia-reperfusion model of the intestine and whether its action is mediated through tissue neutrophils as assessed by myeloperoxidase (MPO) determination. Intestinal ischemia of either 1 or 2 h was induced in rats by clamping the superior mesenteric artery, followed by a 17-min reperfusion period. PTF (25 mg/kg) or saline solution was injected IP 10 min prior to ischemia. Multiple bowel samples were harvested at the end of the reperfusion period and evaluated for histology and tissue MPO. PTF significantly changed the resultant histologic damage to the intestinal mucosa exerted by prolonged ischemia of 1 and 2 h duration, although the beneficial effect of PTF in this animal model was independent of the number of tissue neutrophils as assessed by tissue MPO levels. Pretreatment with PTF can thus reduce the histologic damage caused by prolonged ischemia to the intestine.     

Oxidative damage in fetal rat brain induced by ischemia and subsequent reperfusion. Relation to arachidonic acid peroxidation.

To determine whether ischemia followed by subsequent reperfusion can induce fetal cerebral oxidative damage, we created a model of fetal ischemia/reperfusion using rats at day 19 of pregnancy. Fetal ischemia was induced by unilateral occlusion of the utero-ovarian artery for 20 min. Reperfusion was achieved by releasing the occlusion and restoring the circulation for 30 min. The opposite uterine horn was used as control. We measured brain mitochondrial respiratory control index (RCI) and the concentration of thiobarbituric acid-reactive substances (TBARS) in each group. Arachidonic acid (AA) peroxidation induced by the incubation of brain microvessel fraction and AA was measured. AA peroxidation was also evaluated with and without aspirin, an inhibitor of cyclooxygenase and phenidone, which inhibits both of cyclooxygenase and lipoxygenase. The RCI significantly decreased by the occlusion with (p < 0.01) or without reperfusion (p < 0.05). The TBARS level significantly increased with occlusion plus reperfusion (p < 0.01). AA peroxidation was significantly greater in the occlusion and occlusion plus reperfusion groups than in the control groups (p < 0. 01). Aspirin did not affect peroxidation, while phenidone significantly inhibited it in a concentration-dependent manner (p < 0.001). Accordingly, ischemia followed by reperfusion is likely to induce fetal cerebral lipid peroxidation, which may inhibit mitochondrial respiratory activity. The phenidone-inhibited enzyme lipoxygenase may participate importantly in this peroxidation.     

肾损伤分子-1在急性缺血缺氧再灌注大鼠肾组织中的表达及意义

目的 观察肾损伤分子-1(kidney injury molecule-1,KIM-1)在急性缺血缺氧再灌注肾损伤(acute ischemia reperfusion kidney injury,AIKI)大鼠肾组织中的表达及分布规律,探讨其在诊断急性肾损伤(acute kidney injury,AKI)中的价值.方法 采用清洁级SD大鼠128只,随机分为对照组和模型组,模型组按国际标准建立大鼠AIKI模型,分别于2h、6h、24h、48h、72h、1周、2周、4周处死(n=8),取肾组织,常规HE染色,参照Sayhan等标准对肾小管间质损伤进行半定量评分;免疫组织化学、Western blot法检测KIM-1蛋白的表达及分布;生化法测定血清肌酐(serum creatinine,Scr)水平.结果 (1)大鼠缺血再灌注后2h即出现明显肾小管间质损伤,随着再灌注时间延长损伤加重,48h达高峰后逐渐减轻,但仍高于对照组(P<0.01);(2)Western blot和免疫组织化学检测发现,缺血再灌注后2h肾组织KIM-1的表达明显升高,KIM-1表达水平与肾小管间质损伤评分呈显著正相关(r=0.887,P=0.003);(3)大鼠缺血再灌注后2h Scr明显升高,48h达到最高值后降至正常,其升高与肾小管间质损伤评分无相关性(r=0.280,P=0.502).结论 AIKI模型中大鼠肾组织KIM-1蛋白表达水平显著增加,其表达水平与肾小管间质损伤评分呈正相关,与Scr相比,KIM-1可能为更准确地反映肾损伤情况的指标.