胃癌根治术病人围术期异体输血后外周血单核细胞CD40L表达的变化

目的 研究胃癌根治术病人围手术期异体输血外周血单核细胞(PBMCs)白细胞分化抗原40配体(CD40L)表达的变化。方法 胃癌根治术病人30例,随机分为3组,每组10例。A组围术期不输血,B组围术期输入去白细胞的全血,C组围术期输入异体全血。另选10例健康人作为对照。分别在手术前、术后2、5、10 d采外周静脉血5 ml,用Ficoll分离液梯度离心法分离出PBMCs和血浆,将PBMCs置于自身血浆环境中,并在植物血凝素(PHA,20 mg/L)的刺激下进行培养,48 h后收获细胞,用流式细胞术检测CD40L表达。结果 健康人外周血未受PHA刺激时检测不到CD40L的表达,经PHA刺激后CD40L 细胞占CD4 T细胞的百分数为1.7％±0.4％,与三组胃癌病人术前比较差异无显著性(P>0.05)。与术前比较,B组术后2 d PBMCs CD40L表达升高(P<0.05),C组术后各时点升高(P<0.05);与A组比较,B组术后2 d升高(P<0.05),C组术后各时点升高(P<0.05);与B组比较,C组术后各时点升高(P<0.05)。结论 围手术期异体输血可造成免疫抑制,输异体血后CD40L表达增加,且输全血比输去白细胞的全血更明显。围手术期成分输血优于输注全血。     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

The immunohistology of CD40 in human oral epithelium in health and disease

BACKGROUND: CD40 has a role in the regulation of immune responses, cell proliferation and migration, and apoptosis. Little is known of its distribution in oral mucosal pathology. METHODS: Oral keratinocyte lines were tested for CD40 protein by Western blotting. Immunohistochemistry was used to stain paraffin sections of oral mucosa in health and in inflammatory, reactive, dysplastic and malignant disease. RESULTS: Western blotting confirmed the presence of CD40 in oral keratinocytes. CD40 was generally expressed by keratinocytes in the basal layer, with variable parabasal expression. Langerhans cells also stained positively. Expression was lost in nine of 33 (27%) epithelial dysplasias, seven of which were severe. Eighty-one percent of well, 69% of moderately and 50% of poorly differentiated oral squamous cell carcinomas (OSCC) expressed CD40. Overall, 45 of 65 (69%) OSCC were positive. The pattern of expression was unrelated to tumour differentiation. CONCLUSION: CD40 expression by basal and parabasal oral keratinocytes is physiological. Expression is lost in approximately one-third of oral epithelial dysplasias and OSCC. The significance of such loss remains unknown, but may be related to immunological or other abnormalities of keratinocyte homeostasis.     

不同时间等容血液稀释对犬急性心肌梗塞左室功能的改善作用

在麻醉开胸纯氧呼吸状态下的犬急性心肌梗塞（ＡＭＩ）模型上，观察以右旋糖酐４０在不同时间（ＡＭＩ前１ｈ、２４ｈ和ＡＭＩ后３０ｍｉｎ）行等容血液稀释对犬ＡＭＩ６ｈ内左室功能（±ｄｐ／ｄｔｍａｘ、ＬＶＳＰ）的改善作用。结果表明：ＡＭＩ后３０ｍｉｎ行血液稀释可使＋ｄｐ／ｄｔ－ｍａｘ明显升高（Ｐ＜０．０５）；而ＡＭＩ前１ｈ、２４ｈ行血液稀释不仅使ＡＭＩ后＋ｄｐ／ｄｔ－ｍａｘ明显升高，ＬＶＳＰ与－ｄｐ／ｄｔｍａｘ也明显升高（Ｐ＜０．０５）。提示：①不同时间行等容血液稀释对犬ＡＭＩ后左室收缩功能均有改善作用；②提前稀释血液不仅改善左室收缩功能，也能改善左室舒张功能。     

CD40-CD40配体与动脉粥样硬化的研究进展

动脉粥样硬化是多种因素导致的慢性疾病,严重威胁人类的健康。炎症介质CD40-CD40L被发现广泛存在于与动脉粥样硬化相关的各种细胞及血小板中,可促进其他炎症因子释放,增加内皮的促凝活性,诱导基质金属蛋白酶表达,与氧化型低密度脂蛋白协同作用促进动脉的粥样硬化和斑块的不稳定,在介导动脉粥样硬化和急性冠状动脉综合征的病理过程中起关键作用。     

电针加委中刺血治疗急性腰椎间盘突出症

目的:探寻治疗急性腰椎间盘突出症的较佳疗法.方法:将100例患者随机分为两组.观察组52例,采用电针疗法,穴取腰阳关、大肠俞、关元俞、小肠俞为主,结合委中附近瘀络刺血治疗;对照组48例,采用牵引配合电针,穴取夹脊穴、肾俞、大肠俞为主,观察两组疗效并进行比较.结果:观察组治愈率为55.8%,愈显率为82.7%,对照组分别33.3%、54.2%,组间差异均有统计学意义(P＜0.05,P＜0.01).结论:电针结合委中附近瘀络刺血治疗急性腰椎间盘突出症疗效显著.     

具有靶向免疫抑制作用新型重组融合蛋白B7-2-PE40KDEL真核表达载体的构建及其生物效应

目的:构建B7-2-PE40KDEL的真核表达载体,探讨通过体内表达重组融合蛋白,特异性杀伤高表达CD28 T细胞,阻断B7∶CD28/CTLA4共刺激信号途径诱导免疫耐受的可能性.方法:以原核表达载体pRSETA-B7-2-PE40KDEL质粒为模板,采用PCR及酶切连接的方法构建真核表达载体pcDNA3.1/Zeo( )-B7-2-PE40KDEL.利用RT-PCR、Western 印迹及ELISA法从mRNA、蛋白质水平检测了B7-2-PE40KDEL在RPE-CHO真核细胞中的表达情况.采用MTT法对其特异性杀伤高表达CD28 T细胞的生物活性进行测定.结果:成功构建了pcDNA3.1/Zeo( )-B7-2-PE40KDEL真核表达载体,转染入RPE-CHO细胞后可转录翻译为重组融合毒素蛋白,相对分子质量约为71×103,平均106个转染细胞24 h表达0.23 μg/L.活性测定显示真核载体所表达的B7-2-PE40KDEL可特异性地抑制高表达CD28的人T淋巴细胞系,而对CD28阴性的人白血病细胞系的抑制率较低.结论:真核载体表达的B7-2-PE40KDEL具有良好的靶向性免疫抑制活性,为进一步开展其体内特异性防治移植排斥反应及自身免疫性疾病奠定了基础.     

NEP1-40和甲基强的松龙联合治疗对脊髓修复的影响

目的：探讨甲基强的松龙（MP）和NEP1-40联合治疗对大鼠脊髓损伤后脊髓的功能恢复的影响。方法：选用SD大鼠60只,随机分为联合治疗组、MP治疗组、NEP1-40治疗组和对照组4组。建立大鼠中段胸部脊髓后半部横切模型。MP的给药方法为术后30 min内经鼠尾静脉给予MP 30 mg/kg,后给予剂量5.4 mg/（kg.h）,持续23 h;NEP1-40的给药方法为术后3 d于硬膜下管给予NEP1-40 12.5μg/（20μl PBS.d）,连续7 d。对照组给予等量生理盐水。不同时间点进行运动诱发电位（MEP）测定和行为学评价。结果：联合治疗组大鼠潜伏期延迟时间较MP、NEP1-40治疗组和对照组短,5 w时接近正常,其P1波的潜伏时间为5.42 ms,N1波的潜伏时间为5.55 ms（P〈0.01）,其BBB运动评分5 w时为17分（P〈0.01）;联合治疗组的空洞面积百分比不到对照组的一半（P〈0.01）;NF200阳性染色的神经元数目为20.19个/1000μm^2。结论：MP和NEP1-40联合治疗可减少病变范围,减轻白质纤维脱髓鞘病变,增多NF200阳性神经元数目,促进神经再生,改善由于脊髓后半横切所引发的脊髓电生理的障碍,促进了脊髓功能恢复。在治疗脊髓损伤时,MP与NEP1-40有协同作用,促进脊髓功能恢复。