NLRP3炎性体与中性粒细胞在心肌缺血/再灌注损伤中的交流

炎性体是识别危险模式或病原模式的信号平台,炎性体主要分为2大类:点头样受体(NLR)家族和PYHIN家族。炎性体与多种疾病有关,包括各种感染性疾病、炎症性疾病以及缺血再灌注损伤(ischemia reperfusion injury,IRI)等。炎性体与心肌缺血再灌注损伤是目前的研究热点之一。中性粒细胞作为数量最多的骨髓源性细胞,在无菌性炎症及固有免疫传导通路中发挥着重要作用。在缺血再灌注损伤过程中,死亡的心肌细胞释放大量促炎介质,导致炎性体的活化以及中性粒细胞的聚集。我们综述了NLRP3炎症小体在心肌缺血再灌注损伤中的作用,以及在此病理生理过程中NLRP3与中性粒细胞间的信息交流。     

七叶皂苷钠对肠缺血/再灌注肠过氧化损伤的影响

目的：探讨七叶皂苷钠对肠缺血/再灌注肠过氧化损伤的影响及其机制。方法：复制大鼠肠缺血/再灌注（I/R）损伤模型,观察七叶皂苷钠对血浆和肠组织超氧化物歧化酶（SOD）、丙二醛（MDA）、二胺氧化酶（DAO）、髓过氧化物酶（MPO）的影响,同时观察肠组织水肿和病理损害。结果：七叶皂苷钠可显著改善肠损伤,降低肠组织湿/干比值及含水率,同时升高血浆和肠组织SOD活性,降低血浆和肠组织MPO活性及MDA含量（P〈0.01）。结论：七叶皂苷钠对肠I/R后肠黏膜具有保护作用,其机制可能与抑制中性粒细胞的聚集与活化,对抗脂质过氧化损伤有关。     

重组人源Kunitz型蛋白酶抑制剂治疗大鼠脑皮质缺血/再灌注损伤

目的旨在研究人源重组丝氨酸酶抑制剂rh KD/APP治疗大鼠脑皮质缺血/再灌注损伤的临床前景。方法构建大鼠大脑中动脉(MCAO)局灶性脑缺血/再灌注(I/R)的动物模型,分别用三个剂量rh KD/APP(4、8、16 mg/kg)的干预进行临床治疗,设神经保护药物尼莫地平治疗作为阳性对照,各干预治疗组分别进行临床评分、神经病理损伤、脑水肿程度的评估和比较,评价rh KD/APP在大鼠脑缺血/再灌注神经保护的临床疗效。同时,分组检测缺血/再灌注脑皮质的自由基氧化程度的三个指标(抗氧化酶SOD活性、Na+-K+-ATP酶活性、膜脂过氧化产物丙二醇MDA含量)、反映中性粒细胞呼吸爆发的髓过氧化物酶MPO活性、血管内皮表达粘附因子ICAM-1和E-selectin的表达水平以及损伤区神经元凋亡的状况。结果低、中、高剂量组rh KD/APP干预均能改善脑缺血/再灌注损伤大鼠的临床症状、脑水肿和神经病理损伤,且呈一定量效关系。与缺血/再灌注模型组大鼠比较,各个剂量的rh KD/APP干预均能提高损伤区脑组织抗氧化酶SOD和Na+-K+-ATP酶活性,降低丙二醇MDA含量,降低髓过氧化酶MPO活性,下调粘附因子ICAM-1和E-selectin的表达,拮抗受损神经元的凋亡。与尼莫地平治疗组比较,在降低MPO活性上,三个剂量rh KD/APP均显示出显著优势(P0.05)。其余各个检测指标,rh KD/AP干预组与尼莫地平治疗组之间比较,差异无显著性。结论重组人源rh KD/APP丝氨酸酶抑制剂能够对大鼠脑缺血/再灌注神经损伤发挥保护作用,这些保护作用可能通过清除自由基、抑制中性粒细胞激活和炎性损伤,拮抗神经元凋亡等多层面综合完成。因此,人源Kunitz型丝氨酸蛋白酶抑制剂可成为一个潜在的神经保护药物。     

脊髓缺血再灌注损伤的防治概况

脊髓缺血-再灌注损伤(SCII)是一种严重的神经系统损伤,是缺血脊髓组织恢复血液灌注后,脊髓组织的损伤反而加重,表现为其神经损害体征和形态学改变较前更加明显,其发生机制是多因素的综合结果,治疗措施也具有多样性,脊髓缺血后脊髓微血管结构及功能的破坏和脊髓水肿等是脊髓功能损害的主要诱因,至今为止,脊髓缺血再灌注损伤的防治主要有药物及物理治疗等方法,本文作者通过查阅中外文献对脊髓缺血再灌注损伤的特征、发生机制及防治措施作一综述,希望对研究脊髓缺血再灌注损伤防治的学者能有所帮助。     

持续灌注和静态保存对中性粒细胞凋亡的影响

为研究体外循环机持续灌注、间断压力灌注、单纯低温保存犬离体肺对支气管肺泡灌洗液中中性粒细胞凋亡变化以及对肺泡巨噬细胞吞噬凋亡中性粒细胞的影响,探索最佳的离体肺保存方式,将30只Mongrel犬随机分成3组,为体外循环组、压力灌注组和低温保存组,每组10只。在保持机械通气的条件下,完整摘取双肺,3种不同方式保存离体肺,并按时间点留取支气管肺泡灌洗液标本。流式细胞仪检测犬离体肺支气管肺泡灌洗液中中性粒细胞凋亡,免疫组织化学法检测犬离体肺肺泡巨噬细胞对凋亡中性粒细胞吞噬。随着犬肺离体时间的推移,各实验组离体肺支气管肺泡灌洗液中凋亡的中性粒细胞明显减少,在每个时间点上,体外循环组中性粒细胞的凋亡最多,压力灌注组中次之,低温保存组中最少。各实验组吞噬凋亡中性粒细胞的巨噬细胞随着离体时间的延长呈逐渐减少的趋势,在肺离体各时间点上,体外循环组中巨噬细胞对凋亡中性粒细胞的吞噬清除优于间断压力灌注组和单纯低温保存组。采用体外循环机持续灌注犬离体肺,能增加中性粒细胞凋亡,促使吞噬细胞吞噬凋亡的中性粒细胞,避免发生凋亡延迟,从而减轻离体肺组织的缺血再灌注损伤,具有较好的肺保护作用。     

青霉胺对缺血后再灌注心肌损伤的保护作用

为了解青霉胺对缺血后再灌注心肌损伤的影响,我们采用Ｌａｎｇｅｎｄｒｏｆ离体大鼠心脏灌注模型,先灌注１５ｍｉｎ后停止灌注,模拟缺血６０ｍｉｎ,然后再灌注６０ｍｉｎ。动物分为对照组及青霉胺处理组（３０ｍＭ）。分别测定缺血前及再灌注后心肌组织内三磷酸腺苷（ＡＴＰ）、谷胱甘肽（ＧＳＨ）及谷胱甘肽氧化酶（ＧＳＨ－Ｐｘ）的含量变化,再灌注过程中冠状动脉血流阻力及冠脉流出液中磷酸肌酸激酶（ＣＰＫ）的释放量。结果显示,青霉胺处理组再灌注后心肌组织的ＡＴＰ、ＧＳＨ、ＧＳＨ－Ｐｘ含量均明显高于对照心肌组织中的含量,而青霉胺处理组在再灌注过程中ＣＰＫ的总释放量及平均冠状血流动脉阻力明显低于对照组ＣＰＫ总释放量及平均冠状动脉血流阻力。提示青霉胺可以减轻缺血后再灌注的心肌的损伤,起到保护作用     

青藤碱抗大鼠肝脏缺血/再灌注损伤作用的机制探讨

目的:观察青藤碱时大鼠肝脏缺血再灌注损伤的影响,探讨其保护大鼠肝脏缺血再灌注损伤作用的机制.方法:通过建立大鼠全肝缺血再灌注损伤模型,应用硝酸酶还原法测定肝脏缺血再灌注后60min血清NO水平变化;测定再灌注60 min后肝组织内MDA和SOD含量变化;再灌注60min取肝组织完成肝组织显微结构的观察.结果:肝脏缺血再灌注损伤后血清NO水平降低;青藤碱能提高再灌注后血清NO水平,且能改善肝脏缺血再灌注损伤的微循环,减轻肝细胞内超微结构的损害程度.结论:青藤碱对大鼠肝脏缺血再灌注损伤有保护作用,其主要作用机制是清除氧自由基和改善微循环.     

胰岛素对大鼠肠缺血再灌注损伤的影响

目的:观察胰岛素对大鼠肠缺血再灌注后小肠组织损伤的影响。方法:雄性SD大鼠40只随机分为4组,每组10只,手术对照组、单纯缺血组、再灌注组、胰岛素干预组。于30min缺血和120min再灌注后,进行组织病理学和生化检测。结果:(1)单纯缺血组肠粘膜损害较手术对照组明显升高(P<0.01),超氧化物歧化酶(SOD)活性无明显变化;(2)再灌注组SOD活性明显降低,与手术对照组和单纯缺血组相比较差异均有显著性(P<0.01);(3)胰岛素组SOD活性与再灌注组相比有明显改善(P<0.01)。结论:肠缺血可以引起肠粘膜损伤,再灌注则可加重这种损伤,胰岛素可以减轻再灌注损伤。     

牛磺酸对大鼠肢体缺血/再灌注后肺损伤时磷脂酶A2的影响

目的:探讨牛磺酸对大鼠肢体缺血/再灌注后肺损伤时磷脂酶A2(PLA2)的影响。方法:实验采用大鼠肢体缺血/再灌注损伤模型,将Wistar大鼠30只随机分为3组(n=10),对照组(control)、单纯缺血/再灌注组(I/R)、牛磺酸 缺血/再灌注组(Tau I/R),分别测定血浆丙二醛(MDA)、黄嘌呤氧化酶(XOD)、超氧化物歧化酶(SOD)以及肺组织Taurine、XOD、SOD、MDA、髓过氧化物酶(MPO)的含量、肺湿/干比值(W/D)和磷脂酶A2(PLA2)的活性。结果:口服牛磺酸可有效地降低肺组织MPO、PLA2和XOD的活性。结论:牛磺酸对大鼠肢体缺血再灌注后肺损伤具有保护作用,其机制之一可能与降低PLA2活性和抑制炎症反应有关。     

缺血后处理降低高胆固醇血症大鼠心肌对缺血/再灌注损伤的易感性及其机制

目的:探讨缺血后处理对高胆固醇血症基础上发生的心肌缺血/再灌注损伤的影响及其可能的机制。方法:建立食源性高胆固醇血症大鼠模型,运用TTC染色、酶活性检测等方法测定缺血/再灌注所致的心肌损伤,用实时定量RT-PCR方法检测心肌组织中低氧诱导因子-1α(HIF-1α)mRNA水平,用Western blot方法检测HIF-1α蛋白水平。结果:高胆固醇血症加重了缺血/再灌注造成的心肌损伤,而缺血后处理显著缩小了高胆固醇血症大鼠缺血/再灌注所致的心梗面积,降低了血清肌酸激酶(CK)的活性,减少了心肌细胞凋亡。同时,缺血后处理提高了高胆固醇血症大鼠缺血心肌组织中HIF-1α的蛋白水平。结论:缺血后处理可以降低高胆固醇血症大鼠心肌对缺血/再灌注损伤的敏感性,其效应与心肌组织中HIF-1α的蛋白水平存在着相关性。     

Pharmacological preconditioning with erythropoietin reduces ischemia–reperfusion injury in the small intestine of rats

AimsConsidering the implications that arose from several recent experimental studies using recombinant human erythropoietin in rodents, erythropoietin has been regarded as a pharmacological preconditioning agent. The purpose of the present study was to evaluate whether erythropoietin has a preconditioning effect against ischemia and reperfusion injury in the small intestine of the rat.Main methodsIntestinal ischemia was induced in male Wistar rats by clamping the superior mesenteric artery for 30 min, followed by reperfusion for 180 min. Recombinant human erythropoietin (1000 or 3000 U/kg) or vehicle was administered intraperitoneally 24 h prior to ischemia. After collection of ileal tissue, evaluation of damage was based on measurements of the accumulation of polymorphonuclear neutrophils by technetium-99m-labeled leukocyte uptake, content of malondialdehyde, reduced glutathione, contractile responses to agonists, and an evaluation of histopathological features in intestinal tissue.Key findingsTreatment with erythropoietin 24 h before ischemia significantly reduced the tissue content of malondialdehyde and increased that of reduced glutathione. Pretreatment also significantly suppressed leukocyte infiltration into the postischemic tissue, as evidenced by the lower content of myeloperoxidase and technetium-99m-labeled leukocytes. Physiological and histopathological improvements were also significant with the rHuEpo treatment.SignificanceResults of the present study indicate that rHuEpo is an effective preconditioning agent in ischemic injury of the small intestine. Protection provided by recombinant human erythropoietin is closely related to the inhibition of oxidative stress and leukocyte infiltration, which might be among the possible protective mechanisms of erythropoietin in intestinal ischemia and reperfusion.     

Complement activation in heart diseases. Role of oxidants

Increasing evidence demonstrated that atherosclerosis is an immunologically mediated disease. Myocardial ischemia/reperfusion injury is accompanied by an inflammatory response contributing to reversible and irreversible changes in tissue viability and organ function. Three major components are recognized as the major contributing factors in reperfusion injury. These are: (1) molecular oxygen; (2) cellular blood elements (especially the neutrophils); and (3) components of the activated complement system. The latter two often act in concert. Endothelial and leukocyte responses are involved in tissue injury, orchestrated primarily by the complement cascade. Anaphylatoxins and assembly of the membrane attack complex contribute directly and indirectly to further tissue damage. Tissue damage mediated by neutrophils can be initiated by complement fragments, notably C5a, which are potent stimulators of neutrophil superoxide production and adherence to coronary artery endothelium. The complement cascade, particularly the alternative pathway, is activated during myocardial ischemia/reperfusion. Complement fragments such as the anaphylatoxins C3a and C5a, are produced both locally and systematically, and the membrane attack complex is deposited on cell membranes and subsequent release of mediators such as histamine and platelet activating factor (PAF), thereby causing an increase in vascular permeability with concomitant manifestation of cellular edema. Complement increases the expression of CD18 on the neutrophils and increases P-selectin expression on the surface of the endothelium. Mitochondria may be a source of molecules that activate complements during ischemia/reperfusion injury to myocardium, providing therewith a stimulus for infiltration of polymorphonuclear leukocytes. Tissue salvage can be achieved by depletion of complement components, thus making evident a contributory role for the complement cascade in ischemia/reperfusion injury. The complexities of the complement cascade provide numerous sites as potential targets for therapeutic interventions designed to modulate the complement response to injury. The latter is exemplified by the ability of soluble form of complement receptor 1 (sCR1) to decrease infarct size in in vitro models of ischemia/reperfusion injury. The mechanism(s) that initiates complement activation is not clearly known, although loss of CD59 (protectin) from cells compromised by ischemia/reperfusion may contribute to direct damage of the coronary vascular bed by the terminal complement complex. Therapeutic approaches to ischemia/reperfusion injury in general, and especially those involving complements, are at the very beginning and their potential benefits have still to be adequately evaluated. It may be noted that complement activation has both positive and negative effects and, therefore, might be modulated rather than abruptly blunted.     

The effects of resveratrol administration on lipid oxidation in experimental renal ischemia-reperfusion injury in rats

ABSTRACT

We investigated how resveratrol affects lipid oxidation during experimental renal ischemia-reperfusion injury in rats. We used 48 adult male rats assigned to five groups: group 1, control; group 2, renal ischemia; group 3, renal ischemia + reperfusion; group 4, resveratrol + renal ischemia; group 5, resveratrol + renal ischemia + reperfusion. Plasma and renal tissue malondialdehyde (MDA), and erythrocyte and renal tissue glutathione (GSH) levels were measured and histologic changes in the renal tissue were examined. Ischemia-reperfusion affected the MDA-GSH balance adversely and caused histopathological changes in the renal tissue of the ischemia and ischemia + reperfusion groups. Resveratrol treatment normalized MDA and GSH levels as well as the histopathology that occurred in the renal tissue of the ischemia and ischemia + reperfusion groups.     

Superoxide anion production during reperfusion is reduced by an antineutrophil antibody after prolonged cerebral ischemia

Neutrophils may be involved in the pathophysiology of reperfusion injury following cerebral ischemia. One potential mechanism of reperfusion injury by neutrophils is through production of the superoxide anion. We hypothesized that, due to progressive endothelial damage during ischemia, neutrophil activation would be more prominent after longer periods of ischemia prior to reperfusion. Thus, neutrophils would contribute more to pathological processes such as superoxide anion formation after longer than after shorter periods of ischemia. A reversible middle cerebral artery occlusion model in rats was employed and superoxide anion concentration was measured with a cytochrome c coated electrode placed on the cortical penumbral region. Occlusion times were varied from 60 min to 2 h, and neutrophils were inhibited with an antiCD18 antibody administered prior to occlusion. Neutrophil accumulation and reduction with antibody treatment was confirmed immunohistochemically. Superoxide anion (O₂^•−) concentration was detected during the hours following 60 min of occlusion, and increased further with 2 h of occlusion. Treatment with the antiCD18 antibody had no effect on O₂^•− concentration during reperfusion in the 60–90 min occlusion groups, but O₂^•− concentration was significantly lower in the antiCD18 antibody treated group than in the control group during reperfusion after 120 min of ischemia. The antibody also reduced cortical neutrophil accumulation in the 120 min ischemia group. These results indicate for the first time that superoxide production by neutrophils becomes more important with longer periods of ischemia, and other quantitatively less important sources of superoxide predominate with shorter periods of ischemia. This phenomenon may explain some of the variation seen between different models of ischemia with different durations of ischemia when targeting reactive oxygen species, and supports an approach to combination therapy to extend the therapeutic window and reduce the deleterious effects of reperfusion.     

Postischemic injury in isolated rat hearts is not aggravated by prior depletion of myocardial glutathione

The aim of this study was to test the hypothesis that a decreased myocardial concentration of reduced glutathione (GSH) during ischemia renders the myocardium more susceptible to injury by reactive oxygen species generated during early reperfusion. To this end, rats were pretreated with L-buthionine-S,R-sulfoximine (2 mmol/kg), which depleted myocardial GSH by 55%. Isolated buffer-perfused hearts were subjected to 30 min of either hypothermic or normothermic no-flow ischemia followed by reperfusion. Prior depletion of myocardial GSH did not lead to oxidative stress during reperfusion, as myocardial concentration of glutathione disulfide (GSSG) was not increased after 5 and 30 min of reperfusion. In addition, prior depletion of GSH did not exacerbate myocardial enzyme release, nor did it impair the recoveries of tissue ATP, coronary flow rate and left ventricular developed pressure during reperfusion after either hypothermic or normothermic ischemia. Even administration of the prooxidant cumene hydroperoxide (20 M) to postischemic GSH-depleted hearts during the first 10 min of reperfusion did not aggravate postischemic injury, although this prooxidant load induced oxidative stress, as indicated by an increased myocardial concentration of GSSG. These results do not support the hypothesis that a reduced myocardial concentration of GSH during ischemia increases the susceptibility to injury mediated by reactive oxygen species generated during reperfusion. Apparently, myocardial tissue possesses a large excess of GSH compared to the quantity of reactive oxygen species generated upon reperfusion. (Mol Cell Biochem 156: 79-85, 1996)     

Effect of total flavonoid in rabdosia rubescens on tolerant mice models under cerebral anoxia

ObjectiveTo study the protective effect of total flavonoid in rabdosia rubescens on BIT model by brain ischemic tolerance (hereinafter BIT) model of mice.MethodBIT model is used to block bilateral common carotid arteries and to copy BIT model of mice. After 10 min of transient ischemia for rats in preconditioning group, the mice in the nimodipine group and naoluotong capsule group were given the total flavonoid in rabdosia rubescens (300 mg/kg, 150 mg/kg, 75 mg/kg) for gavage, sham operation group, ischemia/reperfusion injury (hereinafter IRI) group and BIT group were fed with the same volume of 0.5% sodium carboxymethyl cellulose (CMC) once a day for 5 days. After administration for 1 h on day 5 (120 h), the rats in the other groups except for the sham operation group were treated with blood flow block for 30 min and reperfusion for 22 h. The serum NSE level were measured and the brain NO content and NOS activity changes was measured to observe the histopathological changes of brain tissue.ResultsBIT models of mice and in rats were both successfully replicated. The total flavonoid in rabdosia rubescens can decrease the mortality of mice, decrease serum NSE level, increase the content of NO and the activity of NOS in the brain tissue of mice, and improve the pathological damage of cortex and hippocampus of mice.ConclusionThe total flavonoid in rabdosia rubescens can stimulate an endogenous protective mechanism by inducing the release of low levels of cytokines NO and NOS, which reduces the release of serum NSE, relieves the brain tissue ischemia-reperfusion injury, and further improves the protection effect of ischemic preconditioning on brain injury. The damage of brain tissue ischemia and reperfusion, and further improve the ischemia Protective effect of preconditioning on brain injury.     

Neutrophils contribute to ischemia/reperfusion injury in rat liver in vivo

To determine the role of neutrophils in the pathogenesis of hepatic ischemia/reperfusion injury, livers from male Fischer rats were subjected to 45 min of no-flow ischemia followed by reperfusion for up to 24 h. Two phases of liver injury were identified, an initial phase during the first hour of reperfusion and a later progression phase with 80 +/- 3% hepatocyte necrosis and an 80-fold increase of neutrophil infiltration in the liver after 24 h. Pretreatment with a monoclonal antibody against neutrophils, which caused consistent neutropenia, protected the liver from reperfusion injury as indicated by 28 +/- 10% necrosis, and 84% reduction of hepatic neutrophil accumulation and a complete recovery of the hepatic ATP content. Our data suggest that the later progression phase of reperfusion injury after hepatic no-flow ischemia is mediated mainly by neutrophils.     

Leukocytes, oxygen radicals, and myocardial injury due to ischemia and reperfusion

Ischemic myocardium generates stimuli for neutrophil chemotaxis before the final extent of irreversible ischemic injury is attained. Reperfusion accelerates the infiltration of ischemic myocardium by neutrophils. Oxygen radicals released by the activated neutrophils may exacerbate the tissue damage caused by ischemia. Neutrophil depletion by antiserum was shown to limit infarct size in dogs undergoing coronary occlusion for 90 minutes followed by reperfusion for 6 or 72 hours, but not in dogs undergoing occlusion for 4 hours. Prostacyclin, which inhibits the generation of superoxide anions by neutrophils, also limited canine myocardial injury despite no effect on collateral blood flow. Iloprost, an analogue of prostacyclin that inhibits neutrophils also reduced infarct size, while SC39902, an analogue that does not inhibit neutrophils, did not alter infarct size. The results suggest that oxygen radicals released by activated neutrophils play a role in the pathophysiology of myocardial injury due to ischemia followed by reperfusion.     

毛蕊异黄酮通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤的研究

目的:探讨毛蕊异黄酮抗脑缺血再灌注损伤的作用是否与抑制calpain-1的表达有关。方法:将SD大鼠随机分为假手术组、模型组以及药物组,采用线栓法建立大鼠大脑中动脉阻断(MCAO)模型,于缺血再灌注前30 min腹腔注射给予20 mg/kg毛蕊异黄酮或等体积的溶剂。再灌注24 h后,行神经功能学评分、脑梗死面积以及神经元凋亡检测;再灌注12 h、24 h时,采用免疫组化和蛋白印迹技术检测大鼠脑皮层calpain-1的表达。结果:与假手术组大鼠比较,MCAO模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率及calpain-1的表达均明显升高(P0.05),而毛蕊异黄酮能够降低模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率以及calpain-1的表达(P0.05)。结论:毛蕊异黄酮可能通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤作用。     

Astragaloside IV protects against focal cerebral ischemia/reperfusion injury correlating to suppression of neutrophils adhesion-related molecules

Inflammation injury plays a key role in the process of cerebral injury induced by ischemia/reperfusion (I/R). Thus, we studied the potential of astragaloside IV, one of the major and active components of the astragalus membranaceous, to protect rat against cerebral inflammation injury elicited by focal cerebral ischemia and reperfusion and related protective mechanisms. The rat model was induced by intraluminal occlusion of the right middle cerebral artery with reperfusion. Animals received astragaloside IV (10 or 20 mg/kg) injections when reperfusion was began to. Neurobehavioral evaluation and infarct assessment were studied. Myeloperoxidase (MPO) and tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by enzyme-linked immunosorbent assay (ELISA). The rates of CD11b/CD18-positive neutrophils were analyzed via flow cytometry. Intercellular adhesion molecule-1 (ICAM-1) and nuclear factor κB (NF-κB) were measured by immunohistochemistry and Western blot. Astragaloside IV improved neurological outcome and reduced infarct volume at 24 h after reperfusion. The protective effect was achieved by preventing neutrophils accumulation in the brain parenchyma demonstrated by significantly reducing the concentration of MPO in brain tissue. Astragaloside IV exerts the protection through remarkably decreasing the percentage of CD11b/CD18-positive neutrophils and down-regulating the expression of intercellular adhesion molecule-1 (ICAM-1), which is partly achieved by strongly attenuating the production of TNF-α and IL-1β and inhibiting level of nuclear factor-κB (NF-κB). We propose an anti-inflammatory mechanism evoked by astragaloside IV by suppression of neutrophils adhesion-related molecules, which exerts neuroprotection against I/R injury.