丹红注射液对脑梗死患者血浆抵抗素和瘦素浓度的影响

目的:观察丹红注射液对脑梗死患者血浆抵抗素和瘦素浓度的影响,探讨丹红注射液用于脑梗死治疗的机制.方法:80例脑梗死患者分为对照组和治疗组,每组40例.对照组接受常规治疗,治疗组接受常规治疗加用丹红注射液治疗.脑梗死患者静脉血在入院时、入院后第1、2、3、7和14d获得,ELISA测定血浆抵抗素和瘦素浓度.结果:治疗前,治疗组美国国立卫生院神经功能缺损评分与对照组比较差异无统计学意义(P>0.05);治疗后,治疗组美国国立卫生院神经功能缺损评分较对照组显著下降(P<0.05).入院时,治疗组血浆抵抗素和瘦素浓度与对照组比较差异无统计学意义(P>0.05),人院后第1、2、3、7和14d,治疗组血浆抵抗素和瘦素浓度显著低于对照组(P<0.05).结论:丹红注射液可能通过抑制脑梗死后炎性反应,从而达到改善神经功能的目的.     

脑梗死患者血浆IL-11的检测及其临床意义

目的：揭示脑梗死患者血浆IL-11浓度,分析其与预后的相关性。方法：对102例健康体检者和102例脑梗死患者,用ELISA检测血浆IL-11浓度,统计分析其水平改变及与预后的相关性。结果：脑梗死患者血浆IL-11浓度（22．6±9．8）pg／ml较健康体检者（11．2±3．6）pg／ml显著升高（P〈0．01）,与人院时美国国立卫生院神经功能缺损评分呈显著正相关（t=8．749,P〈0．01）,是脑梗死1年内预后不良（OR=1．308,95％C1=1．114-1．569,P〈0．01）和死亡（OR=1．517,95％CI=1．218-1．881,P〈0．01）的独立危险因素,可显著预测脑梗死1年内预后不良（曲线下面积=0．864,95％CI=0．827-0．918,P〈0．01）和死亡（曲线下面积=0．889,95％CI=0．845-0．931,P〈0．01）。结论：脑梗死后血浆IL-11显著升高．其水平检测可作为临床宴用的标志物,有助于早期判断脑梗死预后。     

抗Fas的抗体在实验性病毒性心肌炎中作用机制的研究

目的探讨中和型抗Fas的抗体对小鼠柯萨奇病毒性心肌炎的治疗作用及作用机制。方法60只BAIB/c小鼠随机分为4组：1组空白对照组，2组病毒对照组、3组IgG对照组、4组抗Fas抗体治疗组。于接种后第10天每组随机处死小鼠8只，心肌组织切片HE染色了解心肌损伤情况，电镜技术及原位末端标记法（TUNEL）检测心肌细胞凋亡情况，免疫组化方法检测casimse-3的表达，逆转录．聚合酶链反应（RT-PCR）检测心肌组织中easpase-3的mRNA表达。实时定量PCR（RQ-PCR）定量心肌柯萨奇病毒B3（CVB3）mRNA拷贝数。结果（1）病毒对照组可见caspase-3表达和心肌细胞凋亡，且均与心肌病变积分成正相关（r=0．81，P〈0．01；r=0．73，P〈0．05）。（2）抗Fas抗体治疗组小鼠心肌组织病变积分、心肌细胞凋亡率、caspase-3蛋白和mRNA表达及心肌内CVB3 mRNA拷贝数均明显低于病毒对照组（P〈0．05）和IgG对照组（P〈0．05）。结论Fas/FasL途径介导的心肌细胞凋亡参与了病毒性心肌炎的发病过程，凋亡是导致病毒性心肌炎心肌损伤的重要机制之一，抗Fas抗体可降低caspase-3活化和mRNA表达，减少心肌细胞凋亡，降低心肌细胞内病毒复制，使心肌损伤明显减轻。     

血塞通注射液对短暂性脑缺血发作患者血浆IL-6和TNIF-α浓度的影响

目的：观察血塞通注射液对急性短暂性脑缺血发作患者血浆IL-5和TNF-α浓度的影响,探讨血塞通注射液用于短暂性脑缺血发作治疗的机制。方法：70例急性短暂性脑缺血发作患者分为对照组和治疗组,每组35例。对照组接受常规治疗,治疗组接受常规治疗加用血塞通注射液治疗。急性短暂性脑缺血发作患者静脉血在入院时,入院后第1d、第2d、第3d、第5d和第7d获得,ELISA测定血浆IL-6和TNF-α浓度。结果：治疗组基本治愈11例,显效14例,有效8例,无效2例,总有效率94．3％;对照组基本治愈5例,显效6例,有效8例,无效16例,总有效率54．3％。经卡方检验,两组间比较差异有统计学意义（P〈0．05）。入院时,治疗组血浆IL-6和TNF-α浓度与对照组比较差异无统计学意义（P〉0．05）,人院后第1d、第2d、第3d、第5d和第7d,治疗组血浆IL-6和TNF-α浓度显著地低于对照组（P〈0．05）。结论：血塞通注射液可能通过抑制脑炎症反应,从而改善短暂性脑缺血发作患者神经功能。     

丹红注射液治疗UAP患者临床疗效观察及对血浆可溶性Fas及Fas配体浓度的影响

不稳定型心绞痛(UAP)是介于劳累性稳定型心绞痛与急性心肌梗死(AMI)和猝死之间的临床表现[1].细胞凋亡参与UAP的病理生理过程[2].丹红注射液为丹参、红花等提取物的中药注射剂,具有活血化瘀、通脉舒络等功能,常用于UAP的救治[3-5].最近研究显示,丹红注射液具有抗凋亡作用,能抑制体外培养神经元内质网应激所致凋亡[6].本文观察丹红注射液对UAP患者的治疗效果同时揭示其对血浆可溶性Fas及Fas配体浓度的影响,从而探讨其用于UAP治疗的抗凋亡作用.     

Fas、Caspase-3和抗核小体抗体在参与SLE患者淋巴细胞凋亡紊乱中的作用

目的探讨SLE患者免疫功能紊乱与淋巴细胞凋亡信号传导途径异常之间的关系。方法应用流式细胞术测定SLE患者淋巴细胞表面Fas、FasL及细胞质中活化caspase-3的表达率,并测定凋亡细胞百分率（AnnexinV^＋PI^-）和坏死细胞百分率（AnnexinV^＋PI^＋）。应用ELISA方法测定血清中抗核小体抗体浓度。结果与健康对照组相比,稳定期和活动期SLE患者组淋巴细胞中凋亡细胞和坏死细胞百分率均显著增加（P〈0．05）,淋巴细胞表面Fas、FasL及细胞质中活化caspase-3的表达率也显著增加（P〈0．05）。与稳定期SLE患者组相比,活动期SLE患者组淋巴细胞中坏死细胞百分率显著增加（P〈0．05）,凋亡细胞百分率略有增加但无统计学意义（P〉0．05）。活动期患者组淋巴细胞表面Fas、FasL以及细胞质中活化caspase-3的表达率略有增加但无统计学意义（P〉0．05）。活动期SLE患者组抗核小体抗体浓度显著高于健康对照组和稳定期患者组（P〈0．05）。SLE患者凋亡细胞百分率和活化caspase-3的表达率与补体C3浓度水平呈负相关关系（P〈0．05）。结论Fas信号传导通路在SLE患者淋巴细胞凋亡紊乱中发挥了重要作用。caspase-3的活化是早期提示淋巴细胞凋亡的重要信号。SLE患者淋巴细胞凋亡活化程度与疾病活动程度和免疫效应功能紊乱密切相关,而淋巴细胞凋亡异常程度与抗核小体抗体水平的高低密切相关。淋巴细胞凋亡加速在SLE患者免疫病理损伤加重和免疫细胞调控紊乱中扮演了重要角色。     

醒脑静治疗脑梗死96例疗效分析

目的观察醒脑静治疗脑梗死的疗效。方法96例入选的脑梗死患者随机分为2组。对照组48例病人给予常规治疗，观察组48例病人在常规治疗基础上应用醒脑静30mlivgttqd。结果两组间发病时间及神经功能缺陷无显著差异（P〉0．05），治疗后30d，醒脑静治疗组神经功能缺损评分与对照组比较有统计学差异（P〈0．05），观察组血液中的C-反应蛋白含量与对照组比较明显降低（P〈0．05）。结论醒脑静能有效改善急性脑梗死的神经功能缺失，疗效好值得临床推广应用。     

SLE患者外周血中T、B细胞表面Fas和bcl—2表达的研究

目的 探讨活动期SLE患者外周血中T、B细胞表面Fas和bcl-2的表达水平及其与T、B细胞凋亡的关系。方法 采用流式细胞术,测定活动期SLE患者外周血T、B细胞表面Fas和bcl-2的表达,并同时测定患者血中T、B细胞的凋亡。结果 ①活动期SLE患者外周血中B细胞及CD8T细胞表面bcl-2的表达明显高于正常人（分别为P＜0．05）和P＜0．01）;CD4^ 及CD8^ T细胞表面Fas的表达高于正常人（分别为P＜0．05和P＜0．01）;B细胞表面Fas的表达降低（P＜0．01）;CD4^ T细胞bcl-2的表达下降（P＜0．01）。②活动期SLE患者血中B细胞的凋亡率明显下降,CD8^ T细胞数校正常对照组增加,CD4^ T细胞低于正常人（分别为：P＜0．01、P＜0．05和P＜0．01）。结论 SLE患者体内淋巴细胞凋亡的异常与T、B细胞表面Fas和bcl-2基因的表达的异常有关。     

纤溶酶联合治疗进展型脑梗死患者的疗效观察

目的观察纤溶酶联合氯吡格雷与拜阿司匹林治疗进展型脑梗死的临床疗效。方法选取武钢第二职工医院2009年3月至2011年2月确诊的86例进展型脑梗死患者,随机分为治疗组和对照组,治疗组给予氯吡格雷与拜阿司匹林联合纤溶酶治疗,对照组给予氯吡格雷与拜阿司匹林治疗,两组疗程均为14d,比较两组患者的神经功能缺损程度评分、临床疗效、血液流变学指标以及毒副作用和安全性。结果两组治疗后神经功能缺损程度评分均改善,但治疗组（13．98±1．02）明显优于对照组（17．11±0．96）,差异有统计学意义（P〈0．05）;治疗组显效率及总有效率分别为72．50％、92．5％,明显高于对照组的56．52％、81．8％,差异均有统计学意义（P〈0．05）;治疗后两组患者高切粘度、低切粘度、血浆粘度和纤维蛋白原含量均降低（P〈0．05）,治疗组明显优于对照组。两组患者间毒副作用和安全性比较差异无统计学意义（P〉0．05）。结论纤溶酶联合氯吡格雷与拜阿司匹林治疗进展型脑梗死近期疗效显著．可以作为临床上治疗进展型脑梗死患者的一种有效方法。     

可溶性Fas表达水平与人黑色素瘤相关性的初步研究

目的:分析可溶性Fas(soluble Fas,sFas)表达水平与人黑色素细胞瘤恶性程度的关系,探讨Fas、Fas配体与可溶性Fas在调控细胞凋亡信号转导途径中的作用.方法:对35位确诊黑色素细胞癌患者的皮肤组织标本和病例进行回顾性分析和归类,用免疫荧光的方法检测组织中Fas/FasL的表达水平.通过酶联免疫吸附反应(ELISA)方法对人血清中sFas的浓度进行分析.结果:35例黑色素细胞癌组织中,病理分型浅表型2例、结节型9例、肢端型18例、雀斑痣型6例.Fas在正常皮肤组织中高表达,恶性黑色素癌组织中低表达；而相反FasL在恶性黑色素癌组织中高表达,在正常皮肤组织中表达非常低.可溶性Fas在不同组织中的表达强度差异显著,sFas在恶性黑色素细胞癌患者、良性黑色素瘤和正常人血清中的浓度分别为(36.32±11.57) ng/ml、(7.33±3.78)ng/ml和(4.18±1.88)ng/ml.结论:可溶性Fas在恶性黑色素癌患者血清中含量较高,与黑色素细胞癌恶性程度呈正相关,sFas对细胞凋亡的竞争性抑制可能与黑色素细胞癌的进展密切相关.     

活血通脉汤对大鼠脑缺血再灌注损伤诱导的凋亡蛋白Fas、Caspase-3表达的影响

目的探讨活血通脉汤对大鼠脑缺血再灌注损伤过程中所诱导的凋亡蛋白Fas、Caspase-3表达的影响。方法制作脑缺血再灌注模型，80只大鼠随机平均分为4组，假手术组、模型组、阿司匹林组、活血通脉汤组，每组20只。应用免疫组织化学方法分别检测每组大鼠脑缺血再灌注12、24h脑组织Fas、Caspase-3表达的情况。结果模型组大鼠脑缺血再灌注12、24h脑组织Fas、Caspase-3表达水平明显高于假手术组（P〈0．01）；活血通脉汤组大鼠各时间点脑组织Fas、Caspase-3表达水平明显低于模型组（P〈0．05，P〈0．01），且与阿司匹林组无显著差异性（P〉0．05）。结论活血通脉汤能降低大鼠脑组织Fas、Caspase-3表达水平，减轻缺血脑组织神经元坏死的程度，对大鼠脑缺血再灌注损伤具有保护作用，机制与降低Fas、Caspase-3表达水平有关。     

不稳定型心绞痛病人血清sFas、sFasL及sIL-2R水平的临床价值

目的　探讨血清sFas、sFasL和sIL 2R水平与不稳定型心绞痛 (Unstableanginapectoris,UAP)之间的关系。方法　应用酶联免疫吸附双抗体夹心 (ELISA)法 ,测定了 32例UAP病人 (UAP组 )和 2 0例对照组受试者血清sFas、sFasL和sIL 2R水平。结果　UAP组病人血清sFas和sIL 2R水平均明显高于对照组 (P <0 .0 1) ,而 2组sFasL水平无显著性差别 (P >0 .0 5 )。UAP组病人sFas水平与sIL 2R水平存在显著正相关 (r=0 .4 4 7,P <0 .0 5 )。结论　高水平的血清sFas、sIL 2R与UAP有关。高水平的血清sFas可能通过维持自身免疫炎性反应而导致UAP的发生发展     

Serum levels of soluble Fas ligand in patients with silicosis

Certain patients with silicosis have been reported to exhibit immunological abnormalities such as the appearance of antinuclear antibodies and the occurrence of autoimmune diseases. Fas ligand (FasL) is a type II membrane protein which induces apoptosis by binding to its membrane receptor, Fas. FasL is converted to a soluble form by a metalloproteinase-like enzyme. We have already found serum soluble Fas (sFas) levels in silicosis patients as well as in patients with systemic lupus erythematosus (SLE) to be significantly higher than those in healthy volunteers. To examine further the role of the Fas/FasL system in silica-induced immunological abnormalities, we investigated serum soluble FasL (sFasL) levels in silicosis patients with no clinical symptoms of autoimmune diseases, using ELISA for sFasL. Although the serum sFasL levels in patients with SLE were significantly higher than those in healthy volunteers and showed a slight positive correlation with serum sFas levels, those in silicosis patients exhibited no significant difference from those in healthy volunteers, and there was no correlation with serum sFas levels. However, sFasL levels were elevated in silicosis patients with slight dyspnoea or normal PCO2 among various clinical parameters of silicosis. It may be speculated that the immunological disturbances presented by the abnormalities of apoptosis-related molecules in silicosis patients do not occur with a similar degree of respiratory involvement. Further studies are required to clarify which kinds of factors are involved in silicosis patients who exhibit immunological abnormalities.     

Alteration of Fas and Fas ligand expression during human visceral leishmaniasis

Several studies in murine systems have suggested a role of apoptosis in the pathogenesis of leishmaniasis. However, the role of apoptosis in visceral leishmaniasis in man has not been explored. In this study, we show that patients with visceral leishmaniasis demonstrate significant dysregulation of Fas and Fas ligand. Levels of soluble Fas (sFas) and soluble Fas ligand (sFasL) were elevated in plasma of patients with active visceral leishmaniasis (VL) and individuals co-infected with VL-HIV-1 compared to healthy controls. The levels of sFas and sFasL were normalized 6 months after successful treatment. In VL patients, the expression of membrane bound Fas, and to a lower extent FasL, were up-regulated on Leishmania donovani-infected spleen cells, the site of parasite multiplication. Expression of Fas and FasL on peripheral blood mononuclear cells was within normal range, probably reflecting that the blood is not a normal site of L. donovani infection. Furthermore, this is suggested by the finding that in vitro infection of macrophages with L. donovani up-regulated Fas expression on the surface of infected cells and enhanced the levels of sFasL in supernatants from infected cultures. How this dysregulation may affect the pathogenesis of human visceral leishmaniasis is discussed.     

丹红注射液联合骨髓间充质干细胞移植治疗大鼠脑梗死

背景：单纯骨髓间充质干细胞移植修复受损脑组织的作用并不十分理想。 目的：观察丹红注射液联合骨髓间充质干细胞移植治疗大鼠脑梗死的效果。 方法：用线栓法制备大鼠大脑中动脉阻塞模型,随机分为3组,模型组尾静脉注射PBS、丹红注射液组尾静脉注射2 mL/kg丹红注射液、联合治疗组联合注射2 mL/kg丹红注射液+2.0×10⁹ L^-1的骨髓间充质干细胞悬液,连续5 d,1次/d。 结果与结论：在骨髓间充质干细胞移植后2周,联合治疗组神经功能评分明显优于模型组及丹红注射液组(P < 0.05);移植后3周联合治疗组大鼠脑梗死体积明显小于模型组和丹红注射液组(P < 0.05);病理组织学观察也可见联合治疗组的组织损伤减轻程度大于丹红注射液组和模型组。结果可见丹红注射液联合骨髓间充质干细胞移植治疗大鼠脑梗死疗效显著,可以对脑细胞起到保护作用。     

The soluble form of Fas molecule is elevated in parkinsonian brain tissues

Fas is an apoptosis-signaling receptor molecule on the surface of a number of cell types. The soluble form of Fas (sFas) was measured for the first time in brain (caudate nucleus, putamen and cerebral cortex), ventricular cerebrospinal fluid (VCSF), and lumbar CSF (LCSF) from control and parkinsonian patients by a highly sensitive two-site sandwich enzyme-linked immunosorbent assay (ELISA). The concentrations of sFas in nigro-striatal dopaminergic regions were significantly higher in parkinsonian patients than those in controls, whereas this product in cerebral cortex showed no significant difference between parkinsonian and control subjects. Neither VCSF nor LCSF contained the sFas molecule in the detectable amounts (<16 pg/ml). These results suggest that the presence of sFas possibly leads to cell death/neurodegeneration in parkinsonian brain.     

Fas and fas ligand are up-regulated in pulmonary edema fluid and lung tissue of patients with acute lung injury and the acute respiratory distress syndrome

Apoptosis mediated by Fas/Fas ligand (FasL) interaction has been implicated in human disease processes, including pulmonary disorders. However, the role of the Fas/FasL system in acute lung injury (ALI) and in the acute respiratory distress syndrome (ARDS) is poorly defined. Accordingly, we investigated both the soluble and cellular expression of the Fas/FasL system in patients with ALI or ARDS. The major findings are summarized as follows. First, the soluble expression of the Fas/FasL system was assessed in undiluted pulmonary edema fluid and simultaneous plasma. Pulmonary edema fluid obtained from patients with ALI or ARDS (n = 51) had significantly higher concentrations of both soluble Fas (27 ng/ml; median; P < 0.05) and soluble FasL (0.125 ng/ml; P < 0.05) compared to control patients with hydrostatic pulmonary edema (n = 40; soluble Fas, 12 ng/ml; soluble FasL, 0.080 ng/ml). In addition, the concentrations of both soluble Fas and soluble FasL were significantly higher in the pulmonary edema fluid of the patients with ALI or ARDS compared to simultaneous plasma samples (soluble Fas, 16 ng/ml; soluble FasL, 0.058 ng/ml; P < 0.05), indicating local release in the lung. Higher soluble Fas concentrations were associated with worse clinical outcomes. Second, cellular expression of the Fas/FasL system was assessed by semiquantitative immunofluorescence microscopy in lung tissue obtained at autopsy from a different set of patients. Both Fas and FasL were immunolocalized to a greater extent in the patients who died with ALI or ARDS (n = 10) than in the patients who died without pulmonary disease (n = 10). Both proteins were co-expressed by epithelial cells that lined the alveolar walls, as well as by inflammatory cells and sloughed epithelial cells that were located in the air spaces. Semiquantitative immunohistochemistry showed that markers of apoptosis (terminal dUTP nick-end labeling, caspase-3, Bax, and p53) were more prevalent in alveolar wall cells from the patients who died with ALI or ARDS compared to the patients who died without pulmonary disease. These findings indicate that alveolar epithelial injury in humans with ALI or ARDS is in part associated with local up-regulation of the Fas/FasL system and activation of the apoptotic cascade in the epithelial cells that line the alveolar air spaces.