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1.
《药学学报(英文版)》2020,10(9):1634-1645
Systematic administration of anti-inflammatory cytokine interleukin 4 (IL-4) has been shown to improve recovery after cerebral ischemic stroke. However, whether IL-4 affects neuronal excitability and how IL-4 improves ischemic injury remain largely unknown. Here we report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia–reperfusion (I/R) injury. In multi-electrode array (MEA) recordings, IL-4 reduces spontaneous firings and network activities of mouse primary cortical neurons. IL-4 mRNA and protein expressions are upregulated after I/R injury. Genetic deletion of Il-4 gene aggravates I/R injury in vivo and exacerbates oxygen-glucose deprivation (OGD) injury in cortical neurons. Conversely, supplemental IL-4 protects Il-4−/− cortical neurons against OGD injury. Mechanistically, cortical pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic hyperexcitability and enhanced excitatory synaptic transmissions in Il-4−/− mice. Furthermore, upregulation of Nav1.1 channel, and downregulations of KCa3.1 channel and α6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4−/− mice. Taken together, our findings demonstrate that IL-4 deficiency results in neural hyperexcitability and aggravates I/R injury, thus activation of IL-4 signaling may protect the brain against the development of permanent damage and help recover from ischemic injury after stroke. 相似文献
2.
Roberto V.P. Ribeiro Mitesh V. Badiwala Danny Ramzy Laura C. Tumiati Vivek Rao 《The Journal of thoracic and cardiovascular surgery》2019,157(2):615-625.e1
Objective
Hypertonic saline (HTS) has potent immune and vascular effects. We assessed recipient pretreatment with HTS on allograft function in a porcine model of heart transplantation and hypothesized that HTS infusion would limit endothelial and left ventricular (LV) dysfunction following transplantation.Methods
Heart transplants were performed after 6 hours of cold ischemic storage. Recipient pigs were randomized to treatment with or without HTS (7.5% NaCl) before cardiopulmonary bypass (CPB). Using a myograft apparatus, coronary artery endothelial-dependent (Edep) and -independent (Eind) relaxation was assessed. LV performance was determined using pressure-volume loop analysis. Pulmonary interleukin (IL)-2, IL-6, and tumor necrosis factor (TNF)-α expression was measured.Results
Weaning from CPB and LV performance after transplantation were improved in HTS-treated animals. Successful weaning from CPB was greater in the HTS-treated hearts (8 of 8 vs 2 of 8; P < .05). Mean LV functional recovery was improved in the HTS-treated animals, as assessed by preload recruitable stroke work (65 ± 10% vs 27 ± 10%; P < .001) and end-systolic elastance (55 ± 7% vs 37 ± 4%; P < .001). Treatment with HTS resulted in improved Edep (mean maximum elastance [Emax], 56 ± 5% vs 37 ± 7%; P < .001) and Eind (mean Emax%, 77 ± 6% vs 52 ± 4%; P < .001) vasorelaxation compared with control. Pulmonary expression of IL-2, IL-6, and TNF-α increased following transplantation, whereas HTS therapy attenuated IL production (P < .001). Transplantation increased plasma TNF-α levels and LV TNF-α expression, whereas HTS prevented this up-regulation (P < .001).Conclusions
Recipient HTS pretreatment preserves allograft vasomotor and LV function, and HTS therapy limits CPB-induced injury. HTS may be a novel recipient intervention to prevent graft dysfunction. 相似文献3.
经鼻给予抗ICAM-1抗体对大鼠脑缺血再灌注损伤的保护作用 总被引:1,自引:0,他引:1
目的 探讨经鼻腔给予抗细胞间黏附分子-1(ICAM-1)单克隆抗体(单抗)对大鼠脑缺血再灌注损伤的保护作用.方法 将30只雄性Wistar大鼠随机分为假手术组、脑缺血再灌注组及脑缺血再灌注+经鼻给予高、中、低剂量抗ICAM-1单抗干预组.采用插线法制作局灶脑缺血再灌注模型.各干预组于缺血1 h经鼻给予抗ICAM-1单抗,再灌24 h后取脑行冠状切片.采用TTC、HE及免疫组化染色法测定脑梗死体积及免疫组化阳性区占总面积比.结果 缺血再灌注组脑标本均可见缺血侧的脑膜充血,脑组织肿胀;单纯脑缺血再灌注组及低、中、高抗ICAM-1单抗干预组脑梗死体积(以像素值表示)分别为57 042±12 483、32 871±4 325、25 932±3 103和15 325±3 356,免疫组化阳性区面积占总面积比分别为(6.64±0.476)%、(5.15±0.987)%、(4.36±0.682)%和(3.42±0.537)%,各组间差异均有统计学意义.结论 (1)脑缺血再灌注可使脑组织ICAM-1表达显著增高;(2)经鼻腔给予抗ICAM-1单抗可有效降低脑组织ICAM-1的表达,缩小脑梗死体积;(3)经鼻腔给予抗ICAM-1单抗的剂量同脑梗死体积呈负相关;(4)脑缺血再灌注时ICAM-1免疫组化阳性区面积比与脑梗死体积呈正相关. 相似文献
4.
A. Nakao H. Toyokawa A. Tsung M. A. Nalesnik D. B. Stolz J. Kohmoto A. Ikeda K. Tomiyama T. Harada T. Takahashi R. Yang M. P. Fink K. Morita A. M. K. Choi N. Murase 《American journal of transplantation》2006,6(10):2243-2255
Carbon monoxide (CO), a byproduct of heme catalysis, was shown to have potent cytoprotective and anti-inflammatory effects. In vivo recipient CO inhalation at low concentrations prevented ischemia/reperfusion (I/R) injury associated with small intestinal transplantation (SITx). This study examined whether ex vivo delivery of CO in University of Wisconsin (UW) solution could ameliorate intestinal I/R injury. Orthotopic syngenic SITx was performed in Lewis rats after 6 h cold preservation in control UW or UW that was bubbled with CO gas (0.1-5%) (CO-UW). Recipient survival with intestinal grafts preserved in 5%, but not 0.1%, CO-UW improved to 86.7% (13/15) from 53% (9/17) with control UW. At 3 h after SITx, grafts stored in 5% CO-UW showed improved intestinal barrier function, less mucosal denudation and reduced inflammatory mediator upregulation compared to those in control UW. Preservation in CO-UW associated with reduced vascular resistance (end preservation), increased graft cyclic guanosine monophosphate levels (1 h), and improved graft blood flow (1 h). Protective effects of CO-UW were reversed by ODQ, an inhibitor of soluble guanylyl cyclase. In vitro culture experiment also showed better preservation of vascular endothelial cells with CO-UW. The study suggests that ex vivo CO delivery into UW solution would be a simple and innovative therapeutic strategy to prevent transplant-induced I/R injury. 相似文献
5.
腺苷与异丙酚预处理对犬心肌缺血再灌注损伤的保护作用 总被引:2,自引:0,他引:2
目的探讨腺苷与异丙酚预处理对犬心肌缺血再灌注损伤的保护作用。方法 21只杂种犬,雌雄不拘,随机分为3组(n=7):缺血再灌注组(A组)、异丙酚预处理组(B组)、异丙酚与腺苷联合预处理组(C组)。A组冠状动脉的左前降支结扎60min后松开结扎,再灌注:120min;B组缺血前30min经静脉以5.6mg·kg-1·h-1速率持续泵注异丙酚30min;C组缺血前10min经主动脉根部一次性注入腺苷(10mmol·L-1,10ml),其余处理同B组。记录心脏血液动力学指标,并行节段性室壁运动评分(RWMS)。结果缺血即刻出现了缺血性心电图的变化。与基础值比较,A组缺血期及再灌注期 LVEDP升高,CO、SV、LVEF、CPP、RPP降低,再灌注期MAP降低,HR减慢,B、C组上述缺血再灌注诱导的血液动力学变化减弱,A组缺血期及再灌注期RWMS增加,但B、C组缺血期RWMS低于A组(P< 0.05或0.01)。结论异丙酚预处理对犬心肌缺血再灌注损伤有一定的保护作用,腺苷预处理并未增强其保护作用。 相似文献
6.
大鼠小肠缺血再灌注后血中NO,SOD浓度及肺中Bax,Bcl-2表达的改变 总被引:11,自引:4,他引:7
目的:研究大鼠小肠缺血再灌注后后血中一氧化氮(NO),超氧化物歧化酶(SOD)的浓度变化以及肺组织中Bax,Bcl-2的表达,探讨小肠缺血再灌注后对肺组织的损伤,方法:建立小肠缺血再灌注模型,分对照 ,再灌注后0,30min,1,2h,1,3,7d共8组,于各时点检测血中Bax,Bcl-2的表达情况。结果:大鼠小肠缺血再灌注后NO浓度0min明显升高,2h时降低,随后升高,7d时达高峰,SOD浓度0min明显下降,2h 时升高,随后下降,7d时达最低,Bax,Bcl-2免疫阳性细胞主要位于肺组织中血管内皮细胞和肺泡上皮细胞,再灌注0min,Bax,Bcl-2阳性细胞率增多,30min时Bax,Bcl-2阳性细胞率均升高分别为17.1%和78.1%,Bcl-2表达高于Bax,两者差别显著(P<0.01),2h时降低,其后升高,7d时阳性细胞率达高峰分别为94.1%和83.4%,Bax表达明显高于Bcl-2,两者差异显著(P<0.01)。结论:大鼠小肠缺血再灌注后可引起血中NO,SOD的浓度变化和Bax及Bcl-2阳性细胞在肺组织中的表达改变并可能引起肺组织细胞凋亡和损伤。 相似文献
7.
Dr. Med. Wolfgang Rutsch Horst Schmutzler 《Cardiovascular and interventional radiology》1986,9(5-6):245-252
Reestablishing myocardial perfusion during evolving myocardial infarction may limit the ultimate extent of infarction if viable
myocardial tissue is present when recanalization of the occluded vessel is achieved. This will result in improved left ventricular
function and decreased mortality. In addition to their therapeutic benefits, recanalization procedures have contributed greatly
to our knowledge of acute myocardial infarction. It has been demonstrated that myocardial infarction most often occurs after
thrombotic occlusion of a coronary artery. This has settled a controversy that has preoccupied cardiologists for decades.
Selective intracoronary administration of fibrinolytic agents is followed by recanalization in approximately 80% of cases.
Therapeutic failures are attributable to occlusion caused by other factors, to inactivation of streptokinase by high antibody
concentrations, and to insufficient concentrations of streptokinase at the thrombus as a results of unfavorable flow conditions.
This study is dedicated to Prof. Dr. Med. Horst Schmutzler on the occasion of his 60th birthday. 相似文献
8.
醒脑静注射液对脑缺血再灌注小鼠记忆功能的保护作用 总被引:5,自引:0,他引:5
目的:观察醒脑静(XNJI)对脑缺血再灌注后小鼠记忆功能的保护作用。方法:采用暂时性阻断两侧颈总动脉的方法制备小鼠脑缺血再灌注损伤的模型。测试其被动回避能力,脑内抗氧化酶活性及小鼠断头喘气时间,结果:XNJI可延长脑缺血再灌注小鼠的避暗潜伏期,减少错误次数,并提高谷胱甘肽过氧化物酶(GSH-Px)的活性。延长小鼠断头喘气时间。结论:XNJI可明显减轻脑缺血再灌注导致的小鼠学习记忆功能障碍状态。其主要机制可能与抗氧化作用有关。 相似文献
9.
抑肽酶预处理防护大鼠肝脏缺血再灌注损伤的实验研究 总被引:5,自引:1,他引:4
目的 探讨抑肽酶预处理对肝脏缺血再灌注损伤的防护作用。方法 SD大鼠80只,随机分为抑肽酶预处理和生理盐水预处理两组,观察肝脏缺血再灌注损伤引起及抑肽酶预处理的影响。结果 拟肽酶预处理组大鼠缺血再灌注损伤引起的血清谷丙转氨酶(ALT),谷草转氨酶(AST)活性及肝组织丙二醛(MDA)含量变化均显著低于生理盐水预处理组(P<0.01);肝细胞形态学异常改变也明显较生理盐水预处理组轻。结论 抑肽酶预处理对大鼠肝脏缺血再灌注损伤有明显的防治作用。 相似文献
10.
目的 探讨乏氧心肌显像剂99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)用于诊断实验性缺血心肌的价值.方法 建立大鼠心肌在体缺血再灌注模型,采用体外放射自显影法检测正常对照组(6只)、缺血再灌注组(8只)及无再灌注组(8只)鼠心肌对99Tcm-HL91的摄取.结果 对照组和无再灌注组心肌未见局灶性放射性浓聚,再灌注组心肌非坏死区有较高放射性浓聚,与正常心肌组织的摄取比值为1.634±0.354.结论 99Tcm-HL91表现出较强的亲乏氧组织特性,能较好区分存活和梗死心肌. 相似文献