期刊文献+
共找到14,692篇文章
< 1 2 250 >
每页显示 20 50 100
Effect of Intravenous Ibuprofen on Ischemia-Reperfusion Injury Following Perioperative Tourniquet in Patients Undergoing Total Knee Arthroplasty 认领
1
作者 T. Dulkadiroğlu Ş. M. Aksoy +7 位作者 G. Uğur E. Erkılıç A. D. Özcan S. Erdoğan A. But C. Nural O. Tecimel H. Kara 《麻醉学期刊(英文)》 2021年第1期12-24,共13页
Oxidative stress occurs in the organism with ischemia due to tourniquet use and subsequent reperfusion. Oxidative stress increases postoperative morbidity. Some Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) perform t... Oxidative stress occurs in the organism with ischemia due to tourniquet use and subsequent reperfusion. Oxidative stress increases postoperative morbidity. Some Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) perform their anti-inflammatory effects in part by binding or inhibiting their formation of active oxygen radicals at the site of inflammation. In this study, we aimed to evaluate the effect of IV ibuprofen on ischemia-reperfusion injury (IRI) in patients undergoing total knee arthroplasty over oxidative stress parameters.<span> </span><span>The patients were randomly divided into two groups. Each patient</span><span>’</span><span>s protocol number, age, sex, body mass index (BMI), additional disease, drug use, tourniquet time, hemoglobin value, additional analgesic requirement and application, adverse reaction development on the first postoperative day were recorded in the research follow-up form. Both groups of patients;before anesthesia, 45 minutes after tourniquet application, 5 minutes after tourniquet lowering, 20 minutes after tourniquet lowering and at 24th-hour post-op;TOS, TAS, paraoxonase, arylesterase, myeloperoxidase, catalase, ceruloplasmin, albumin, IMA, thiol-disulfide balance tests were studied. Statistical analysis of test results was performed.</span><span> </span><span>We observed that antioxidants decreased and oxidants increased on the first postoperative day in both groups in patients who underwent total knee arthroplasty. The decrease in antioxidant parameters was higher in IV ibuprofen doses compared to the control group in the case group;these doses indicate that the drug adversely affects the organism in the fight against oxidative stress, which is an undesirable effect. To evaluate this negative effect of IV ibuprofen which is increasingly used in postoperative analgesia, studies with different doses of drugs and different surgeries may be needed.</span> 展开更多
关键词 ISCHEMIA-REPERFUSION IV Ibuprofen Oxidative Stress Knee Arthroplasty Non-Steroidal Anti-Inflammatory Drugs
在线阅读 免费下载
RTN1-C mediates cerebral ischemia/reperfusion injury via modulating autophagy 认领
2
作者 Jun Ling Haijian Cai +3 位作者 Muya Lin Shunli Qi Jian Du Lijian Chen 《生物化学与生物物理学报:英文版》 SCIE CAS 2021年第2期170-178,共9页
It has been widely accepted that autophagic cell death exacerbates the progression of cerebral ischemia/reperfusion (I/R). Our previous study revealed that overexpression of reticulon protein 1-C (RTN1-C) is involved ... It has been widely accepted that autophagic cell death exacerbates the progression of cerebral ischemia/reperfusion (I/R). Our previous study revealed that overexpression of reticulon protein 1-C (RTN1-C) is involved in cerebral I/R injury. However, the underlying mechanisms have not been studied intensively. This study was designed to evaluate the effect of RTN1-C on autophagy under cerebral I/R. Using an in vitro oxygen-glucose deprivation followed by reoxygenation and a transient middle cerebral artery occlusion model in rats, we found that the expression of RTN1-C protein was significantly upregulated. We also revealed that RTN1-C knockdown suppressed overactivated autophagy both in vivo and in vitro, as indicated by decreased expressions of autophagic proteins. The number of Beclin-1/propidium iodide-positive cells was significantly less in the LV-shRTN1-C group than in the LV-shNC group. In addition, rapamycin, an activator of autophagy, aggravated cerebral I/R injury. RTN1-C knockdown reduced brain infarct volume, improved neurological deficits, and attenuated cell vulnerability to cerebral I/R injury after rapamycin treatment. Taken together, our findings demonstrated that the modulation of autophagy from RTN1-C may play vital roles in cerebral I/R injury, providing a potential therapeutic treatment for ischemic brain injury. 展开更多
关键词 cerebral ischemia/reperfusion AUTOPHAGY RTN1-C RAPAMYCIN
Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury 认领 被引量:1
3
作者 Ulrich Goebel Stefanie Scheid +4 位作者 Sashko Spassov Nils Schallner Jakob Wollborn Hartmut Buerkle Felix Ulbrich 《中国神经再生研究:英文版》 SCIE CAS 2021年第1期192-198,共7页
We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STA... We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STAT3)and nuclear factor kappa B(NF-κB)are also affected by argon and may play a role in neuroprotection.It also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain inflammation.Despite intensive research,the further exact mechanism remains unclear.In this study,human neuroblastoma cells were damaged in vitro with rotenone over a period of 4 hours(to mimic cerebral ischemia and reperfusion damage),followed by a 2-hour post-conditioning with argon(75%).In a separate in vivo experiment,retinal ischemia/reperfusion injury was induced in rats by increasing intraocular pressure for 1 hour.Upon reperfusion,argon was administered by inhalation for 2 hours.Argon reduced the binding of the transcription factors signal transducer and activator of transcription 3,nuclear factor kappa B,activator protein 1,and nuclear factor erythroid 2-related factor 2,which are involved in regulation of neuronal damage.Flow cytometry analysis showed that argon downregulated the Fas ligand.Some transcription factors were regulated by toll-like receptors;therefore,their effects could be eliminated,at least in part,by the TLR2 and TLR4 inhibitor oxidized phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine(OxPAPC).Argon treatment reduced microglial activation after retinal ischemia/reperfusion injury.Subsequent quantitative polymerase chain reaction analysis revealed a reduction in the pro-inflammatory cytokines interleukin(IL-1α),IL-1β,IL-6,tumor necrosis factorα,and inducible nitric oxide synthase.Our results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial activation.Argon has no known side effects o 展开更多
关键词 ARGON ischemia/reperfusion injury MICROGLIA NEUROINFLAMMATION NEUROPROTECTION noble gas SH-SY5Y toll-like receptor transcription factor
在线阅读 下载PDF
miR-133b-3p对大鼠脑缺血/再灌注损伤的影响及其作用机制 认领
4
作者 高静贵 徐琛 +5 位作者 秦振秀 瞿祥 吴双 梁程伟 谢晓云 刘竞丽 《广西医科大学学报》 CAS 2021年第1期35-41,共7页
目的:探讨miR-133b-3p对脑缺血/再灌注(I/R)损伤大鼠的影响。方法:将36只雄性SD大鼠随机分为6组,每组6只,分别为假手术组、I/R组、I/R+miR-133b-3p激动剂(agomir)组、I/R+miR-133b-3p抑制剂(antagomir)组、I/R+agomir阴性对照(NC)组、I/... 目的:探讨miR-133b-3p对脑缺血/再灌注(I/R)损伤大鼠的影响。方法:将36只雄性SD大鼠随机分为6组,每组6只,分别为假手术组、I/R组、I/R+miR-133b-3p激动剂(agomir)组、I/R+miR-133b-3p抑制剂(antagomir)组、I/R+agomir阴性对照(NC)组、I/R+antagomir NC组。采用实时荧光定量PCR(qPCR)法检测大鼠脑组织miR-133b-3p表达水平,苏木精-伊红(HE)染色观察大鼠脑组织病理形态变化,原位末端标记(TUNEL)染色检测神经元细胞凋亡,利用DIANA数据库筛选miR-133b-3p的靶基因,通过生物信息学方法对靶基因的上、下游完整调控机制进行分析。结果:与假手术组比较,I/R组大鼠神经行为学评分显著升高(P<0.01),脑组织miR-133b-3p表达水平明显降低(P<0.05);与相应NC组比较,I/R+agomir组行为学评分显著升高,miR-133b-3p表达明显升高,而I/R+antagomir组miR-133b-3p表达显著降低(均P<0.01)。与I/R组比较,I/R+agomir组神经元损伤严重,神经元细胞萎缩,核深染且形状不规则,细胞凋亡率明显升高(P<0.01);相反,I/R+antagomir组神经元损伤少,神经元细胞核染适中且均匀,神经元凋亡率明显降低(P<0.01)。KEGG通路富集分析发现,靶基因主要作用于自噬信号通路和MAPK信号通路等,上游转录因子和激酶富集结果显示miR-133b-3p主要与UBTF和MAPK1等因子相关。结论:miR-133b-3p可能通过调控自噬通路和MAPK信号通路加重大鼠脑I/R损伤,抑制miR-133b-3p表达对大鼠神经元有保护作用。 展开更多
关键词 miR-133b-3p 缺血/再灌注 生物信息学
在线阅读 免费下载
运动预处理对脑缺血再灌注大鼠VEGF、NeuN蛋白表达的影响 认领
5
作者 裴飞 王雪冬 +2 位作者 李宝龙 唐强 朱路文 《康复学报》 2021年第1期37-43,共7页
目的:探索运动预处理对于脑缺血再灌注大鼠血管内皮生长因子(VEGF)、神经元核心抗原(NeuN)蛋白表达的影响。方法:采用随机数字表法将大鼠分为假手术组、模型组、运假组(运动预处理与假手术组)和运模组(运动预处理与模型组),每组24只。... 目的:探索运动预处理对于脑缺血再灌注大鼠血管内皮生长因子(VEGF)、神经元核心抗原(NeuN)蛋白表达的影响。方法:采用随机数字表法将大鼠分为假手术组、模型组、运假组(运动预处理与假手术组)和运模组(运动预处理与模型组),每组24只。每组按再灌注24 h、3 d后又分为2个亚组,每个亚组12只。造模前,运假组和运模组行跑台训练3周。模型组和运模组大鼠采用改良Longa线栓法制备大鼠大脑中动脉阻塞(MCAO)模型,造模2 h后将线栓缓慢拔出至颈总动脉主干分叉处。假手术组和运假组大鼠造模方法同上,但线栓仅从颈总动脉插入约10 mm以后即拔出,不能阻塞大脑中动脉血流供应。采用改良神经功能评分(mNSS)评估神经功能;免疫组化和蛋白质免疫印迹分别测定缺血侧脑组织VEGF和NeuN蛋白表达水平。结果:①假手术组和运假组未出现神经功能缺损表现,与模型组比较,运模组在再灌注24 h、3 d后神经功能缺损评分降低,组间比较差异有统计学意义(P<0.05)。②在VEGF表达方面,再灌注24 h后,假手术组可见少量的VEGF表达,阳性细胞胞体小,突起细;与运模组阳性率(14.40%)相比,假手术组阳性率(4.70%)、模型组阳性率(9.80%)、运假组阳性率(8.80%)均较低,且差异均有统计学意义(P<0.05)。再灌注3 d后,与运模组阳性率(23.80%)相比,假手术组阳性率(5.40%)、模型组阳性率(12.40%)、运假组阳性率(14.20%)均降低,且差异均有统计学意义(P<0.05)。③在NeuN蛋白表达水平方面,再灌注24 h后,与运模组相比,模型组表达较少,差异有统计学意义(P<0.05);再灌注3 d后,与运模组相比,模型组表达较少,差异有统计学意义(P<0.05)。结论:脑缺血再灌注前给予运动预处理可减少脑缺血再灌注以后的神经功能缺损表现,通过增强VEGF与NeuN的蛋白表达,从而改善感觉运动功能障碍和运动行为。 展开更多
关键词 缺血再灌注 血管内皮生长因子 神经元核心抗原 运动预处理
在线阅读 免费下载
Activated PKB/GSK-3β synergizes with PKC-δ signaling in attenuating myocardial ischemia/reperfusion injury via potentiation of NRF2 activity: Therapeutic efficacy of dihydrotanshinone-Ⅰ 认领
6
作者 Hao Zengy Lingling Wangy +6 位作者 Jiawei Zhang Ting Pan Yinghua Yu Jingxia Lu Ping Zhou Hua Yang Ping Li 《药学学报:英文版》 SCIE CAS 2021年第1期71-88,共18页
Disrupted redox status primarily contributes to myocardial ischemia/reperfusion injury(MIRI).NRF2,the endogenous antioxidant regulator,might provide therapeutic benefits.Dihydrotanshinone-Ⅰ(DT)is an active component ... Disrupted redox status primarily contributes to myocardial ischemia/reperfusion injury(MIRI).NRF2,the endogenous antioxidant regulator,might provide therapeutic benefits.Dihydrotanshinone-Ⅰ(DT)is an active component in Salvia miltiorrhiza with NRF2 induction potency.This study seeks to validate functional links between NRF2 and cardioprotection of DT and to investigate the molecular mechanism particularly emphasizing on NRF2 cytoplasmic/nuclear translocation.DT potently induced NRF2 nuclear accumulation,ameliorating post-reperfusion injuries via redox alterations.Abrogated cardioprotection in NRF2-deficient mice and cardiomyocytes strongly supports NRF2-dependent cardioprotection of DT.Mechanistically,DT phosphorylated NRF2 at Ser40,rendering its nuclear-import by dissociating from KEAP1 and inhibiting degradation.Importantly,we identified PKC-δ-(Thr505)phosphorylation as primary upstream event triggering NRF2-(Ser40)phosphorylation.Knockdown of PKC-δdramatically retained NRF2 in cytoplasm,convincing its pivotal role in mediating NRF2 nuclear-import.NRF2 activity was further enhanced by activated PKB/GSK-3βsignaling via nuclear-export signal blockage independent of PKC-δactivation.By demonstrating independent modulation of PKC-δand PKB/GSK-3β/Fyn signaling,we highlight the ability of DT to exploit both nuclear import and export regulation of NRF2 in treating reperfusion injury harboring redox homeostasis alterations.Coactivation of PKC and PKB phenocopied cardioprotection of DT in vitro and in vivo,further supporting the potential applicability of this rationale. 展开更多
关键词 DihydrotanshinoneⅠ NRF2 Cytoplasmic/nuclear translocation PKC-δ PKB/GSK-3β/Fyn Phosphorylation Redox homeostasis Ischemia/reperfusion injury
葱白提取物对心肌缺血再灌注损伤模型大鼠心肌细胞凋亡的作用及机制研究 认领
7
作者 杨剑锋 柯于鹤 +1 位作者 雷杰 田立群 《江汉大学学报:自然科学版》 2021年第1期30-36,共7页
目的探讨葱白提取物(FOB)对心肌缺血再灌注损伤模型(I/R)大鼠心肌细胞凋亡的保护作用及机制。方法36只雄性SD大鼠随机分为sham组(n=12)、I/R组(n=12)和FOB组(n=12)。结扎左冠状动脉前降支45 min再灌注。多导生理记录仪记录左心室功能变... 目的探讨葱白提取物(FOB)对心肌缺血再灌注损伤模型(I/R)大鼠心肌细胞凋亡的保护作用及机制。方法36只雄性SD大鼠随机分为sham组(n=12)、I/R组(n=12)和FOB组(n=12)。结扎左冠状动脉前降支45 min再灌注。多导生理记录仪记录左心室功能变化,TUNEL染色观察心肌细胞凋亡情况,计算心肌细胞凋亡率;Western blot检测心肌梗死区,梗死边缘区,未梗死区pp38、p53蛋白表达;RT-PCR检测心肌组织p38、p53 mRNA表达量。结果与sham组相比,I/R组心功能显著受损,同时细胞凋亡率增加,p-p38、p53蛋白表达量显著升高,p53 mRNA相对表达水平显著升高(P<0.05);FOB预处理后改善了大鼠心功能,同时细胞凋亡率降低,p-p38、p53蛋白表达量下降,p53 mRNA相对表达水平下调(P<0.05)。结论FOB具有改善I/R模型大鼠心功能作用,其机制与调节p38 MAPK信号通路蛋白表达、抗心肌细胞凋亡相关。 展开更多
关键词 葱白提取物 缺血再灌注 细胞凋亡 p38 MAPK
在线阅读 免费下载
金钱草提取物通过调控miR-129-5p表达对脑缺血再灌注大鼠脑损伤的保护作用 认领
8
作者 阚桐 王越 王瑞刚 《中国药师》 CAS 2021年第1期12-15,69,共5页
目的:探讨金钱草提取物对脑缺血再灌注大鼠脑损伤的保护作用及分子机制。方法:将大鼠随机分为7组:假手术组、缺血再灌注组、金钱草提取物低、中、高剂量组(300,600,900 mg·kg^(-1))、金钱草提取物+anti-miR-NC组(900 mg·kg^(-... 目的:探讨金钱草提取物对脑缺血再灌注大鼠脑损伤的保护作用及分子机制。方法:将大鼠随机分为7组:假手术组、缺血再灌注组、金钱草提取物低、中、高剂量组(300,600,900 mg·kg^(-1))、金钱草提取物+anti-miR-NC组(900 mg·kg^(-1))、金钱草提取物+anti-miR-129-5p组(900 mg·kg^(-1)),每组9只。除假手术组外,其余各组建立大鼠大脑中动脉闭塞局灶性脑缺血模型。建模成功后,各给药组灌胃给予相应剂量药物,假手术组及缺血再灌注组给予等量生理盐水。采用神经行为缺损评分评估脑损伤情况,氯化三苯基四氮唑染色法检测脑梗死体积,采用检测试剂盒分别检测丙二醛(MDA)含量及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性,采用酶联免疫吸附实验(ELISA)试剂盒分别检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)含量,实时荧光定量PCR检测微小核糖核酸(miR)-129-5p表达水平。结果:与假手术组相比,缺血再灌注组大鼠神经行为评分、脑梗死体积、MDA、TNF-α、IL-1β、IL-6含量显著升高,SOD、CAT活性及miR-129-5p表达水平显著降低(P<0.05);与缺血再灌注组相比,金钱草提取物低、中、高剂量组大鼠神经行为评分、脑梗死体积、MDA、TNF-α、IL-1β、IL-6含量显著降低,SOD、CAT活性及miR-129-5p表达水平显著升高,且呈剂量依赖性(P<0.05)。干扰miR-129-5p表达逆转了金钱草提取物对缺血再灌注大鼠脑损伤的保护作用。结论:金钱草提取物可能通过上调miR-129-5p抑制脑缺血再灌注大鼠脑损伤。 展开更多
关键词 金钱草提取物 微小核糖核酸-129-5p 缺血再灌注 脑损伤
活络通脑片对大鼠脑缺血再灌注损伤的治疗作用 认领
9
作者 林艳霞 张胜杰 +3 位作者 耿海局 王权 马仁强 陈健文 《中南药学》 CAS 2021年第1期38-43,共6页
目的探究活络通脑片对大鼠脑缺血再灌注损伤的作用。方法取SPF级雄性Wistar大鼠利用栓线法制备大鼠脑缺血再灌注模型,按照Zea Longa的5分制评分标准进行神经病学评分。将1~3分的模型动物随机分为模型对照组,活络通脑片低、中、高剂量组... 目的探究活络通脑片对大鼠脑缺血再灌注损伤的作用。方法取SPF级雄性Wistar大鼠利用栓线法制备大鼠脑缺血再灌注模型,按照Zea Longa的5分制评分标准进行神经病学评分。将1~3分的模型动物随机分为模型对照组,活络通脑片低、中、高剂量组(85、170、340 mg·kg-1)和阳性对照组(银杏叶片26 mg·kg-1),同法另设假手术组。造模24 h后开始灌胃给药,连续给药14 d。观察活络通脑片对神经功能缺损及行为学评分、血小板活化因子(PAF)诱导的血小板聚集、脑源性神经营养因子(BDNF)、碱性成纤维细胞生长因子(bFGF)表达和脑组织病理学的影响。结果与模型对照组相比,活络通脑片可改善神经功能缺损及行为学评分(P<0.05);可抑制血小板聚集(P<0.05),提高脑组织中bFGF和BDNF的表达(P<0.05),并对脑皮质和海马损伤有一定的改善作用。结论活络通脑片对大鼠脑缺血再灌注损伤有较好的治疗作用。 展开更多
关键词 活络通脑片 缺血再灌注 脑卒中 脑源性神经营养因子 碱性成纤维细胞生长因子
在线阅读 免费下载
川芎嗪通过抑制内质网应激减轻小肠缺血再灌注损伤的研究 认领
10
作者 孔维 尹清臣 《现代消化及介入诊疗》 2021年第1期77-81,共5页
目的研究川芎嗪(TMP)对大鼠小肠缺血再灌注损伤及内质网应激通路的影响。方法将120只Wistar大鼠按照随机数字表法平均分为假手术组、模型组和TMP低、中、高(15、30、60 mg/kg)剂量组。造模前30 min腹腔注射给药,假手术组、模型组腹腔注... 目的研究川芎嗪(TMP)对大鼠小肠缺血再灌注损伤及内质网应激通路的影响。方法将120只Wistar大鼠按照随机数字表法平均分为假手术组、模型组和TMP低、中、高(15、30、60 mg/kg)剂量组。造模前30 min腹腔注射给药,假手术组、模型组腹腔注射生理盐水。通过夹闭肠系膜上动脉60 min制备小肠缺血再灌注大鼠模型,再灌注2 h后,检测肠组织含水量;通过HE染色法行肠组织病理学检查并进行损伤评分(Chiu′s氏评分)、TUNEL法观察细胞凋亡情况并计算凋亡指数(AI);ELISA法检测肠组织CRP、TNF-α、IL-1β含量;Western blot法检测内质网应激相关蛋白(GRP78、CHOP)及Cleved Caspase-12、Cleved Caspase-3、NF-κB蛋白表达。结果与模型组比较,TMP中、高剂量组大鼠肠组织含水量显著降低(P<0.05);肠系膜病变明显改善且凋亡细胞数量明显减少,Chiu′s氏评分和AI显著降低(P<0.01);肠组织CRP、TNF-α、IL-1β含量和GRP78、CHOP、Cleved Caspase-12、Cleved Caspase-3、NF-κB蛋白表达水平均显著降低(P<0.05)。结论TMP能够通过抑制内质网应激相关炎症和细胞凋亡通路,对小肠缺血再灌注损伤起到保护作用。 展开更多
关键词 川芎嗪 内质网应激 小肠 缺血再灌注 炎症 细胞凋亡
在线阅读 下载PDF
小檗碱预处理对大鼠肝缺血再灌注损伤的影响 认领
11
作者 朱虹燕 王胜军 +2 位作者 户占飞 宋健楠 陈雪昭 《中国实验诊断学》 2021年第2期259-263,共5页
目的评价小檗碱在大鼠肝缺血再灌注(HIR)损伤中的作用,以及探讨硫氧还蛋白结合蛋白(TXNIP)/NOD样受体蛋白3(NLRP3)炎症小体信号通路在该过程中所起的作用。方法成年SD大鼠随机分成4组,每组10只。假手术组(S组):生理盐水灌胃2周后仅进行... 目的评价小檗碱在大鼠肝缺血再灌注(HIR)损伤中的作用,以及探讨硫氧还蛋白结合蛋白(TXNIP)/NOD样受体蛋白3(NLRP3)炎症小体信号通路在该过程中所起的作用。方法成年SD大鼠随机分成4组,每组10只。假手术组(S组):生理盐水灌胃2周后仅进行开关腹操作;肝缺血再灌注组(IR组):生理盐水灌胃2周后建立大鼠热HIR模型;小檗碱组(BBR组):小檗碱100mg·kg^(-1)·d^(-1)灌胃2周后建立大鼠热HIR模型;二甲基亚砜组(DMSO组):用DMSO代替小檗碱灌胃,余步骤与小檗碱组相同。再灌注6h后(S组术后6h),收集各组大鼠下腔静脉血和肝脏组织。检测血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST);ELISA法检测白介素-1β(IL-1β)、白介素-18(IL-18);按原位末端转移酶标记技术(TUNEL)染色法检测肝脏组织细胞凋亡情况;免疫组化观察肝脏组织NLRP3蛋白表达情况;蛋白免疫印迹法检测TXNIP、NLRP3、ASC、caspase-1等炎症小体相关蛋白;结果与S组相比,IR组、BBR组和DMSO组血清ALT、AST、IL-1β、IL-18水平显著升高(P<0.05),肝脏组织中NLRP3蛋白表达增多,TXNIP、NLRP3、ASC、caspase-1等炎症小体信号通路相关蛋白显著上调(P<0.05);与IR组和DMSO组相比,BBR组血清ALT、AST、IL-1β、IL-18水平显著下调(P<0.05),细胞凋亡减少,肝脏组织中NLRP3蛋白表达降低,TXNIP、NLRP3、ASC、pro-caspase-1、caspase-1等炎症小体相关蛋白显著下调(P<0.05),IR组和DMSO组无明显差异(P>0.05)。结论小檗碱可以减轻大鼠肝缺血再灌注损伤,其机制可能与抑制TXNIP/NLRP3炎症小体信号通路有关。 展开更多
关键词 肝脏 缺血再灌注 小檗碱 炎症小体
在线阅读 下载PDF
Garciesculenxanthone B induces PINK1-Parkin-mediated mitophagy and prevents ischemia-reperfusion brain injury in mice 认领
12
作者 Man Wu Guang Lu +10 位作者 Yuan-zhi Lao Hong Zhang Dan Zheng Zhao-qing Zheng Juan Yi Qian Xiang Li-ming Wang Hong-sheng Tan Hua Zhou Han-ming Shen Hong-xi Xu 《中国药理学报:英文版》 SCIE CAS 2021年第2期199-208,共10页
Mitophagy is a selective form of autophagy involving the removal of damaged mitochondria via the autophagy-lysosome pathway.PINK1-Parkin-mediated mitophagy is one of the most important mechanisms in cardiovascular dis... Mitophagy is a selective form of autophagy involving the removal of damaged mitochondria via the autophagy-lysosome pathway.PINK1-Parkin-mediated mitophagy is one of the most important mechanisms in cardiovascular disease,cerebral ischemia-reperfusion(I/R)injury,and neurodegenerative diseases.In this study we conducted an image-based screening in YFP-Parkin HeLa cells to discover new mitophagy regulators from natural xanthone compounds.We found that garciesculenxanthone B(GeB),a new xanthone compound from Garcinia esculenta,induced the formation of YFP-Parkin puncta,a well known mitophagy marker.Furthermore,treatment with GeB dose-dependently promoted the degradation of mitochondrial proteins Tom20,Tim23,and MFN1 in YFP-Parkin HeLa cells and SH-SY5Y cells.We revealed that GeB stabilized PINK1 and triggered Parkin translocation to the impaired mitochondria to induce mitophagy,and these effects were abolished by knockdown of PINK1.Finally,in vivo experiments demonstrated that GeB partially rescued ischemia-reperfusion-induced brain injury in mice.Taken together,our findings demonstrate that the natural compound GeB can promote the PINK1-Parkin-mediated mitophagy pathway,which may be implicated in protection against I/R brain injury. 展开更多
关键词 garciesculenxanthone B MITOPHAGY PARKIN PINK1 ischemia-reperfusion injury
瑞舒伐他汀通过UCP2-SIRT3信号调控脑I/R对神经元的损伤 认领
13
作者 云强 董雪佳 +3 位作者 王梦娇 刘雅虹 王智光 江名芳 《中国临床药理学与治疗学》 CAS 2021年第2期144-153,共10页
目的:研究瑞舒伐他汀对脑缺血-再灌注损伤的保护作用及作用机制。方法:(1)建立脑梗死及OGD/R细胞模型,检测不同浓度瑞舒伐他汀对细胞增殖及细胞凋亡的影响;(2)用不同浓度瑞舒伐他汀处理OGD/R细胞模型,观察瑞舒伐他汀对细胞形态和细胞中U... 目的:研究瑞舒伐他汀对脑缺血-再灌注损伤的保护作用及作用机制。方法:(1)建立脑梗死及OGD/R细胞模型,检测不同浓度瑞舒伐他汀对细胞增殖及细胞凋亡的影响;(2)用不同浓度瑞舒伐他汀处理OGD/R细胞模型,观察瑞舒伐他汀对细胞形态和细胞中UCP2/SIRT3表达和定位的影响;(3)构建UCP2沉默的细胞系,观察细胞线粒体形态和细胞中TOMM20及SIRT3分子表达与定位,研究瑞舒伐他汀在OGD/R细胞模型中发挥保护作用的通道和机制;(4)检测线粒体膜电位,PCR检测线粒体生成基因PGC1、Drp1和Opa1表达,研究瑞舒伐他汀对线粒体的保护作用。结果:(1)不同浓度瑞舒伐他汀均可以明显减低OGD/R细胞凋亡,提高细胞存活率;(2)瑞舒伐他汀通过影响细胞UCP2和SIRT3表达,进而发挥细胞保护作用,使细胞免受OGD/R损伤;(3)瑞舒伐他汀通过调控UCP2影响TOMM20表达,增加线粒体跨膜转运和能量代谢,增强线粒体功能,提高细胞存活;(4)瑞舒伐他汀阻止OGD/R细胞膜电位下降,保护线粒体,改善细胞状态,减少细胞凋亡。结论:瑞舒伐他汀通过调控UCP2/SIRT通路来抑制OGD/R细胞线粒体损伤,从而发挥神经元保护作用。 展开更多
关键词 瑞舒伐他汀 UCP2 SIRT3 OGD/R 缺血再灌注
在线阅读 免费下载
LIR损伤过程中腹腔给予氢气的兔血清TRAIL、Omi/HtrA2及骨骼肌组织Omi/HtrA2表达观察 认领
14
作者 刘丹丹 李林 +4 位作者 董云 崔昌盛 庄宝祥 田华 王岱君 《山东医药》 CAS 2021年第6期36-39,共4页
目的观察肢体缺血—再灌注(LIR)损伤过程中腹腔注射氢气的兔血清肿瘤坏死因子-相关凋亡诱导配体(TRAIL)、线粒体丝氨酸蛋白酶(Omi/HtrA2)及骨骼肌组织匀浆上清Omi/HtrA2的水平变化,并探讨其可能作用机制。方法 45只新西兰大耳白兔随机分... 目的观察肢体缺血—再灌注(LIR)损伤过程中腹腔注射氢气的兔血清肿瘤坏死因子-相关凋亡诱导配体(TRAIL)、线粒体丝氨酸蛋白酶(Omi/HtrA2)及骨骼肌组织匀浆上清Omi/HtrA2的水平变化,并探讨其可能作用机制。方法 45只新西兰大耳白兔随机分为LIR+氢气组(H组)、LIR组(I组)及对照组(C组),每组各15只。H、I组将袖带绑缚于兔右后肢根部股动脉搏动处(超过收缩压20~30 mmHg可完全阻断血流),束缚4 h时打开球囊开关(再灌注),H组于再灌注前5 min腹腔注射5 mL/kg氢气,C、I组同时刻腹腔注射等体积空气。C组仅用相同袖带缠缚相同部位。分别于再灌注24、72、168 h时取各组大耳白兔,分别取静脉血及胫骨前肌肌组织,检测血清TRAIL、Omi/HtrA2及骨骼肌组织Omi/HtrA2。结果与I组比较,再灌注24、72、168 h时H组兔血清TRAIL、Omi/HtrA2水平低(P均<0.01);与I组比较,再灌注24、72、168 h时H组兔骨骼肌组织匀浆上清Omi/HtrA2水平降低(P均<0.01)。同组不同时间段I、H组血清TRAIL及其骨骼肌组织匀浆上清Omi/HtrA2间比较,P均<0.01,I组血清Omi/HtrA2间差异有统计学意义(P均<0.01)。结论腹腔注射氢气的LIR损伤兔血清TRAIL、Omi/HtrA2及骨骼肌组组织匀浆上清Omi/HtrA2表达均降低。TRAIL、Omi/HtrA2可能参与LIR的发生发展。氢气可通过抑制TRAIL的活化及血清及骨骼肌Omi/HtrA2释放,抑制细胞凋亡。 展开更多
关键词 肿瘤坏死因子-相关凋亡诱导配体 线粒体丝氨酸蛋白酶 缺血-再灌注 氢气 细胞凋亡
在线阅读 下载PDF
急性下肢缺血再灌注损伤机制的研究进展 认领
15
作者 谷岩 何菊 +1 位作者 侯骊坤 刘辉 《齐齐哈尔医学院学报》 2020年第12期1521-1522,共2页
肢体缺血再灌注的发生可以影响急性机械性创伤患者进行血管外科手术的预后,因此一直是临床上的研究热点,特别是针对病理改变机制的研究。本文此次将目前对于急性下肢缺血再灌注损伤的机制总结并综述如下。
关键词 缺血 缺血再灌注 氧自由基 研究进展
在线阅读 下载PDF
依托咪酯后处理肢体缺血再灌注肺损伤模型大鼠Fas/Fasl通路的变化 认领
16
作者 邹海波 孙晓峰 《中国组织工程研究》 CAS 北大核心 2020年第32期5162-5167,共6页
背景:目前文献已证实依托咪酯预处理可减轻肢体缺血再灌注对远隔脏器造成的损伤,但依托咪酯后处理对肢体缺血再灌注对远隔脏器是否有保护作用及其机制,目前报道甚少。目的:观察依托咪酯后处理对肢体缺血再灌注肺损伤的影响。方法:将大... 背景:目前文献已证实依托咪酯预处理可减轻肢体缺血再灌注对远隔脏器造成的损伤,但依托咪酯后处理对肢体缺血再灌注对远隔脏器是否有保护作用及其机制,目前报道甚少。目的:观察依托咪酯后处理对肢体缺血再灌注肺损伤的影响。方法:将大鼠采用夹闭双侧股动脉2 h、再灌注3 h的方法制备肢体缺血再灌注肺损伤模型,设为模型组;于大鼠肢体缺血2 h后,经尾静脉分别注射依托咪酯1.0 mg/kg或地塞米松0.2,0.5和1.0 mg/kg,分别设为依托咪酯后处理组、地塞米松0.2,0.5,1.0 mg/kg组。各组于再灌注3 h时经颈动脉取血,行动脉血气分析,记录血氧分压。随后取大鼠肺组织采用免疫组织化学染色检测病理变化、应用Hoechst33258染色法检测肺细胞凋亡指数以及检测肺湿/干质量比;应用WestenBlot法和RT-PCR法分别测定肺组织Fas蛋白和Fasl mRNA的表达;采用ELISA法测定肺组织肿瘤坏死因子α及白细胞介素1β水平。结果与结论:①与模型组比较,在依托咪酯后处理组中血氧分压升高(P<0.05),凋亡指数、肺湿/干质量比、Fas和Fasl mRNA表达、肿瘤坏死因子α及白细胞介素1β蛋白表达下降,凋亡坏死的病灶数量减少(P<0.05);②与依托咪酯后处理组比较,在不同剂量地塞米松的3组中,地塞米松0.5 mg/kg组的上述各指标改变均无显著性差异(P>0.05);③上述结果证实,依托咪酯后处理可降低大鼠肢体缺血再灌注导致的肺损伤,其机制可能与下调Fas/Fasl有关;在统计学角度上,依托咪酯1.0 mg/kg降低肺损伤的效价强度,几乎相当于地塞米松0.5 mg/kg。 展开更多
关键词 依托咪酯 后处理 缺血再灌注 Fas Fasl 凋亡指数 氧分压 肿瘤坏死因子α 白细胞介素1β 大鼠
在线阅读 下载PDF
异氟烷对兔脑缺血再灌注损伤的保护作用及机制研究 认领
17
作者 蒋砾 张新疆 《川北医学院学报》 CAS 2020年第5期767-770,共4页
目的:通过研究异氟烷(ISO)预处理对兔脑缺血再灌注损伤的保护作用及机制,为临床治疗脑缺血提供实验依据。方法:取健康雄性兔45只随机分为5组:假手术组(Sham组)、缺血再灌注组(模型组)、1%ISO预处理10 min组(A组)、1.5%ISO预处理10 min... 目的:通过研究异氟烷(ISO)预处理对兔脑缺血再灌注损伤的保护作用及机制,为临床治疗脑缺血提供实验依据。方法:取健康雄性兔45只随机分为5组:假手术组(Sham组)、缺血再灌注组(模型组)、1%ISO预处理10 min组(A组)、1.5%ISO预处理10 min组(B组)及2%ISO预处理10 min组(C组),每组各9只。线栓法制备脑缺血再灌注损伤模型,缺血2 h再灌注24 h后对其进行以下实验:(1)神经功能损害评估Zeal Longa5及NSS评分;(2)氯化三苯基四氮唑(TTC)染色检测脑梗死体积;(3)免疫组织化学检测测定脑内NF-κBP56蛋白的表达;(4)流式细胞术检测细胞凋亡数;(5)脑中脑皮质组织超氧化物歧化酶(SOD)活性的变化。结果:模型组Longa5评分、脑梗死体积、脑内NF-κBP56含量均大于其它组(P<0.05),C组各项指标低于其它两组,差异有统计学意义(P<0.05);A、B、C组脑中SOD活性均略低于Sham组,其中C组与Sham组最为接近,模型组脑中SOD活性明显低于A、B、C组与Sham组。Sham组细胞凋亡比例低于A、B、C组及模型组(P<0.05)。结论:异氟烷对兔脑缺血再灌注损伤有明显的保护作用,且在本研究中高剂量ISO作用效果最佳。 展开更多
关键词 异氟烷 脑损伤 缺血再灌注 脑梗死 超氧化物歧化酶
在线阅读 免费下载
Gasdermin家族蛋白在缺血再灌注损伤大鼠肾组织中的表达变化 认领
18
作者 邓军辉 谭微 +5 位作者 戚玉竹 蒋易伟 吴志芬 郑卢权 林利容 杨聚荣 《免疫学杂志》 CAS CSCD 北大核心 2020年第5期369-375,共7页
目的研究gasdermin家族蛋白在缺血再灌注(ischemia/reperfusion,I/R)损伤大鼠肾组织中的表达变化,并探讨该家族各蛋白与急性肾损伤(acute kidney injury,AKI)的关系。方法 20只Sprague Dawley(SD)雄性成年大鼠随机分为假手术组与I/R组(n... 目的研究gasdermin家族蛋白在缺血再灌注(ischemia/reperfusion,I/R)损伤大鼠肾组织中的表达变化,并探讨该家族各蛋白与急性肾损伤(acute kidney injury,AKI)的关系。方法 20只Sprague Dawley(SD)雄性成年大鼠随机分为假手术组与I/R组(n=10),分别给予假手术或肾脏缺血再灌注处理后,采集血液及肾组织标本;自动分析仪检测各大鼠血清肌酐、血清尿素氮水平,肾组织PAS染色评估损伤程度;蛋白印迹法检测肾组织中炎症因子interleukin(IL)-1β和interleukin(IL)-18、炎性半胱氨酸蛋白酶caspase-1和caspase-11的前体及活性体、gasdermin家族蛋白(GSDMA、GSDMB、GSDMC、GSDMD、DFNA5、DFNB59)前体及N端的表达水平。结果与假手术组比较,I/R组大鼠血清肌酐、血清尿素氮水平及肾小管损伤评分均显著增加(P<0.000 1);肾组织中IL-1β、IL-18,caspase-1前体及活性体、caspase-11前体及活性体、GSDMD前体及N端表达水平均显著增加(P<0.000 1、P<0.001或P<0.05),且GSDMD表达变化与肾功能损害程度、炎症因子表达变化呈显著正相关(P<0.01),而GSDMA、GSDMB、GSDMC、DFNA5、DFNB59各蛋白前体及N端表达水平均无明显变化(P>0.05)。结论 GSDMD蛋白前体及N端在缺血再灌注损伤大鼠肾组织中表达上调,而GSDMA、GSDMB、GSDMC、DFNA5、DFNB59前体及N端表达无明显差异,提示GSDMD蛋白可能是gasdermin家族中唯一介导AKI肾脏焦亡的成员,其他成员可能并不参与该病理生理过程。 展开更多
关键词 Gasdermin家族 急性肾损伤 缺血/再灌注 细胞焦亡
Involvement of moesin phosphorylation in ischemia/reperfusion induced inner blood-retinal barrier dysfunction 认领
19
作者 Jing Xu Qiong Liu +4 位作者 Ming Ma Lin-Jiang Chen Jian Yu Ke Xiong Jing Wu 《国际眼科杂志:英文版》 SCIE CAS 2020年第4期545-551,共7页
AIM: To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion(RIR) insult.METHODS: C57 BL/6 mice were subjected to continued ischemia ... AIM: To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion(RIR) insult.METHODS: C57 BL/6 mice were subjected to continued ischemia for 45 min, followed by blood reperfusion. The expression and phosphorylation of moesin in retinal vessels were detected by immunohistochemistry and Western blotting. The inner blood-retinal barrier was evaluated using FITCdextran leakage assay on whole-mount retina. Further studies were conducted to explore the effects of p38 mitogen-activated protein kinase(MAPK) pathway on the involvement of moesin in RIR-evoked retinal vascular hyperpermeability response. RESULTS: It revealed that RIR induced moesin phosphorylation in a time-dependent manner after reperfusion. The phosphorylation of moesin was alleviated by inhibitions of p38 MAPK, while this treatment also ameliorated the dysfunction of inner blood-retinal barrier. CONCLUSION: The results suggest that moesin is involved in RIR-evoked retinal vascular endothelial dysfunction and the phosphorylation of moesin is triggered via p38 MAPK activation. 展开更多
关键词 RETINAL ISCHEMIA-REPERFUSION MOESIN p38 MITOGEN-ACTIVATED protein kinase INNER blood-retinal barrier mice
Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53 认领
20
作者 Marwan Almoiliqy Jin Wen +10 位作者 Bin Xu Yu-chao Sun Meng-qiao Lian Yan-li Li Eskandar Qaed Mahmoud Al-Azab Da-peng Chen Abdullah Shopit Li Wang Peng-yuan Sun Yuan Lin 《中国药理学报:英文版》 SCIE CAS CSCD 2020年第9期1208-1222,共15页
Our preliminary study shows that cinnamaldehyde(CA)could protect against intestinal ischemia/reperfusion(I/R)injuries,in which p53 and NF-κB p65 play a synergistic role.In this study,we conducted in vivo and in vitro... Our preliminary study shows that cinnamaldehyde(CA)could protect against intestinal ischemia/reperfusion(I/R)injuries,in which p53 and NF-κB p65 play a synergistic role.In this study,we conducted in vivo and in vitro experiments to verify this proposal.SD rats were pretreated with CA(10 or 40 mg·kg−1·d−1,ig)for 3 days,then subjected to 1 h mesenteric ischemia followed by 2 h reperfusion.CA pretreatment dose-dependently ameliorated morphological damage and reduced inflammation evidenced by decreased TNF-α,IL-1β,and IL-6 levels and MPO activity in I/R-treated intestinal tissues.CA pretreatment also attenuated oxidative stress through restoring SOD,GSH,LDH,and MDA levels in I/R-treated intestinal tissues.Furthermore,CA pretreatment significantly reduced the expression of inflammation/apoptosis-related NF-κB p65,IKKβ,IK-α,and NF-κB p50,and downregulated apoptotic protein expression including p53,Bax,caspase-9 and caspase-3,and restoring Bcl-2,in I/R-treated intestinal tissues.We pretreated IEC-6 cells in vitro with CA for 24 h,followed by 4 h hypoxia and 3 h reoxygenation(H/R)incubation.Pretreatment with CA(3.125,6.25,and 12.5μmol·L−1)significantly reversed H/R-induced reduction of IEC-6 cell viability.CA pretreatment significantly suppressed oxidative stress,NF-κB activation and apoptosis in H/R-treated IEC-6 cells.Moreover,CA pretreatment significantly reversed mitochondrial dysfunction in H/R-treated IEC-6 cells.CA pretreatment inhibited the nuclear translocation of p53 and NF-κB p65 in H/R-treated IEC-6 cells.Double knockdown or overexpression of p53 and NF-κB p65 caused a synergistic reduction or elevation of p53 compared with knockdown or overexpression of p53 or NF-κB p65 alone.In H/R-treated IEC-6 cells with double knockdown or overexpression of NF-κB p65 and p53,CA pretreatment caused neither further decrease nor increase of NF-κB p65 or p53 expression,suggesting that CA-induced synergistic inhibition on both NF-κB and p53 played a key role in ameliorating intestinal I/R injuries.Fina 展开更多
关键词 CINNAMALDEHYDE mesenteric ischemia/reperfusion injury inflammation oxidative stress apoptosis MITOCHONDRIA P53 NF-ΚB
上一页 1 2 250 下一页 到第
使用帮助 返回顶部 意见反馈