多胺的细胞保护作用

细胞损伤时多胺的合成和摄取增加。多胺对多种组织细胞损伤具有直接保护作用，其可能机制包括调节细胞离子平衡；影响胞内信息传导通路；维持细胞内Ｃａ２＋稳态；抑制膜指质过氧化；促进细胞修复等环节。多胺的细胞保护作用具有一定的药理学意义。     

热休克蛋白的分子遗传学研究进展

热休克蛋白是一组在进化上高度保守的蛋白质,是细胞在各种不利于自的因素因素刺激下所表现的一种以因素达和计控方面发生改变的反应,通过此种方式,诱导热休克蛋白的产生而启动内源性保护机制,本主要从细胞和分子水平上扼要介绍热休克蛋白的分子遗传学研究进展及其在整形外科方面的应用。     

Survivin在过氧化氢预处理诱导的适应性细胞保护中的作用

目的探讨H2O2预处理对存活素(survivin)表达的影响及存活素在H2O2预处理的适应性细胞保护中的作用。方法在PC12细胞建立H2O2预处理对抗H2O2诱导细胞凋亡的实验模型,应用甲氮甲唑蓝(MTT)法检测细胞存活率,碘化丙啶(PI)染色流式细胞术检测细胞凋亡率,Hoechst染色检测细胞凋亡的形态学改变,免疫印迹法(Westernblot)测定存活素的表达水平。结果用100μmol/LH2O2预处理PC12细胞90min可明显地抑制300μmol/LH2O2作用12h后引起的细胞毒性和细胞凋亡,并可以显著地上调PC12细胞存活素的表达;JAK2抑制剂AG-490不仅可以抑制存活素的表达,而且拮抗H2O2预处理的适应性细胞保护作用。结论存活素是JAK-STAT通路的靶基因,可能在H2O2预处理诱导的适应性细胞保护机制中起着重要的作用。     

卟啉及金属卟啉化合物对糖分子的作用研究

目的研究卟啉化合物对糖分子的分子识别作用。方法采用荧光滴定法分别对所合成的卟啉化合物及其金属配合物进行糖分子识别研究。结果通过对其结合常数分析,卟啉化合物及其金属配合物对乳糖的识别作用普遍强于葡萄糖,嵌金属Zn,Fe的卟啉化合物其对糖的结合能力明显强于没有金属配位的卟啉化合物。结论卟啉化合物及其金属配合物对糖分子具有选择性识别作用。     

热休克蛋白的分子遗传学研究进展

热休克蛋白是一组在进化上高度保守的蛋白质 ,是细胞在各种不利于自身的因素刺激下所表现的一种以基因表达和调控方面发生改变的反应。通过此种方式 ,诱导热休克蛋白的产生而启动内源性保护机制。本文主要从细胞和分子水平上扼要介绍热休克蛋白的分子遗传学研究进展及其在整形外科方面的应用     

HCV入胞相关分子及其作用机制的研究进展

丙型肝炎病毒(hepatitis C virus, HCV)是一种有包膜的单股正链RNA病毒, 属于黄病毒科丙型肝炎病毒属.包膜病毒感染细胞的初始步骤即是病毒外膜与靶细胞膜相互结合作用的过程, 多种病毒蛋白及宿主细胞分子参与其中.HCV主要的靶细胞是肝细胞, 病毒颗粒首先要通过肝细胞膜进入胞浆才能开始其生命周期.     

JAK-STAT通路调制NF-kB介导H2O2预处理的细胞保护作用

目的:探讨核因子-kB(nuclear factor-kB,NF-kB)在H2O3预处理诱导的适应性细胞保护作用中的作用及JAK-STAT通路对NF-kB的调制.方法:在PC12细胞建立H2O2预处理对抗氧化应激(300 μmol/LH2O2)损伤细胞的实验模型.应用碘化丙啶(PI)染色流式细胞术检测细胞凋亡率,免疫印迹法(Western blotting)测定NF-kB和STAT3的表达水平.结果:用100 μmol/L H2O2预处理PC12细胞90 min可显著地抑制300 μmol/LH2O2作用12 h引起的细胞凋亡,并明显地上调NF-kB和STAT3的表达,NF-kB抑制剂MG-132(10 μmol/L)和JAK2抑制剂AG-490(10 μmol/L)均可抑制H2O2预处理引起的适应性细胞保护作用及上调NF-kB表达的作用.结论:JAK-STAT通路调节NF-kB介导的H2O2预处理的细胞保护作用.     

生物昼夜节律分子机制的研究进展

昼夜节律是生物界最普遍的一种生物节律，与许多生理和行为的过程有关，如睡眠－觉醒周期、体温波动、激素水平等。本文从昼夜节律的分子遗传学基础、节律发生的分子机制、调节机制等方面，对昼夜节律生物钟进行了综述。     

热休克蛋白参与NF-κB介导的H2O2预处理的细胞保护作用

目的探讨热休克蛋白(HSP)是否参与核因子-κB(NF-κB)介导的H2O2预处理的细胞保护作用。方法应用碘化丙啶(PI)染色流式细胞技术(FCM)检测细胞凋亡率,免疫印迹法(Westernblot)测定NF-κB的表达水平,免疫细胞化学染色法测定NF-κB的核转移。结果100μmol/LH2O2预处理PC12细胞90min可显著地抑制300μmol/LH2O2引起的细胞凋亡,并可明显地上调PC12细胞NF-κB的表达及促进NF-κB的核转移,同时也能上调HSP70和HSP90的表达。NF-κB的抑制剂TPCK阻断NF-κB表达,并显著地阻断H2O2预处理的细胞保护作用及HSP70和HSP90的表达。结论HSP70和HSP90参与NF-κB介导的H2O2预处理的适应性细胞保护作用。     

JAK—STAT通路调制NF-κB介导H2O2预处理的细胞保护作用

目的：探讨核因子-κB（nuclearfactor-κB，NF-κB）在H2O2预处理诱导的适应性细胞保护作用中的作用及JAK—STAT通路对NF-κB的调制。方法：在PC12细胞建立H2O2预处理对抗氧化应激（300μmol／LH2O2）损伤细胞的实验模型。应用碘化丙啶（PI）染色流式细胞术检测细胞凋亡率，免疫印迹法（Westem blotting）测定NF-κB和STAT3的表达水平。结果：用1000μmol／L H2O2预处理PC12细胞90min可显著地抑制300panol／L H2O2作用12h引起的细胞凋亡，并明显地上调NF-κB和STAT3的表达，NF-κB抑制剂MG-132（100μmol／L）和JAK2抑制剂AG-490（10izmol／L）均可抑制H2O2预处理引起的适应性细胞保护作用及上调NF-κB表达的作用。结论：JAK-STAT通路调节NF-κB介导的H2O2预处理的细胞保护作用。     

细胞胀亡的研究进展

Oncosis is a special kind of non-apoptotic cell death mode. It is characterized by cellular swelling, organelle swelling, blebbingand increased membrane permeability. More and more attentions pay to the research of this field in recent years. The review discuss the recent advances of oncosis on pathological change, molecular mechanisms and detection approaches．     

海藻糖保护同种带瓣大动脉的最适浓度

背景：目前液氮低温保护组织和器官技术已经非常成熟,但其保护剂一直以来争论不一。 目的：观察不同冷冻保护剂对液氮深低温冻存同种带瓣大动脉组织细胞凋亡和代谢的影响,寻求最佳的冷冻保护剂及冷冻保护剂的最适浓度。 方法：取新西兰大白兔带瓣主动脉、肺动脉标本,将其在液氮中冻存12,15,18个月,冻存液分别使用0.1 mol/L二甲基亚砜,0.1 mol/L海藻糖,0.1 mol/L海藻糖+0.1 mol/L二甲基亚砜,0.2 mol/L海藻糖+0.1 mol/L二甲基亚砜,0.3 mol/L海藻      糖+0.1 mol/L二甲基亚砜。标本复温后,免疫组织化学方法检测标本的细胞凋亡情况,葡萄糖消耗量测定法检测组织细胞的代谢水平。 结果与结论：免疫组织化学和葡萄糖消耗量测定结果均显示经0.1 mol/L海藻糖+0.1 mol/L二甲基亚砜,0.2 mol/L海藻糖+  0.1 mol/L二甲基亚砜冻存液处理的标本冻存效果最好,其次是经0.3 mol/L海藻糖+0.1 mol/L二甲基亚砜处理和经0.1 mol/L海藻糖单独处理的标本,单独使用0.1 mol/L二甲基亚砜处理的标本冻存效果最差。说明海藻糖对液氮深低温保存同种带瓣大动脉活性有很好的保护作用,单独使用海藻糖优于单独使用二甲基亚砜,联合应用海藻糖和二甲基亚砜效果更好,且联合应用的海藻糖最佳浓度范围是0.10~0.20 mol/L。     

pH-responsive polymers for trehalose loading and desiccation protection of human red blood cells

PP-50, a synthetic pH-responsive biopolymer, is here shown to increase the permeability of the phospholipid bilayer to trehalose, a disaccharide accumulated in desiccation tolerant organisms across all kingdoms. Uptake of 251 ± 6 mm intracellular trehalose facilitated an increase in the membrane integrity of vacuum dried cells by a factor of 9 ± 1 and reduced extent of hemoglobin oxidation in dried cells from 66 ± 1% to 23 ± 3%. To elucidate the mechanism of PP-50 mediated trehalose delivery, permeability studies were conducted using molecules ranging in size from sucrose to 10 kDa poly(ethylene glycol). It was shown that the logarithm of relative diffusant membrane permeability decreased linearly with diffusant molecular volume, suggesting transport via non-Stokesian diffusion. Consistent with this conclusion, topographic atomic force micrographs reported membrane thinning proximate to PP-50 adsorption on the erythrocyte membrane, a phenomenon associated with increased incidence of phospholipid hydrocarbon chain bending.     

Alteration of adhesion molecule expression and cellular polarity in hepatocellular carcinoma

AIMS: To study the expression of adhesion molecules in human liver and their possible roles during hepatocarcinogenesis. METHODS AND RESULTS: The expression of adhesion molecules in normal liver tissues, benign including probable premalignant lesions and malignant lesions was systematically investigated by immunohistochemistry and Western blotting. In normal liver, both hepatocytes and bile duct cells expressed symplekin, desmoglein 1/2, desmocollin 2, desmoplakin and plakophilin 2, but did not express desmocollin 1/3 or plakophilin 1. In benign hepatocyte lesions, expression of the adherens junctions and desmosomes was uniform and slightly increased, but symplekin appeared to show reduced expression in dysplastic lesions. In hepatocellular carcinoma (HCC), the expression of adhesion molecules was often heterogeneous and of abnormal location. Tumour cells with an abnormal distribution or loss of adhesion molecules showed an apolar arrangement of tissue architecture. The expression levels of the adhesion molecules correlated with the differentiation grades of HCC cells. CONCLUSIONS: The decreased expression of symplekin may be an early step in the transformation of hepatocytes, whereas alteration of the expression of adherens junctions and desmosomes may indicate more serious changes.     

Recent advances in the cellular and molecular biology of mast cells

The mast cell is now considered to play a pivotal role not only in allergic reactions but also in a number of inflammatory disorders. After immunological activation via the IgE receptor, the mast cell releases a variety of cytokines, lipid-derived mediators, amines, proteases and proteoglycans--all of which can regulate adjacent cells and the metabolism of the extra-cellular matrix of connective tissues. While it had been known for some time that mast cells differ in a number of properties in varied tissue sites, it was not known why or how this heterogeneity occurred. The development of in-vitro techniques to culture mast cells and the reconstitution of mast-cell-deficient mice are two major approaches that have facilitated analyses of how the tissue microenvironment regulates the phenotype of mast cells. In this review by Richard L. Stevens and K. Frank Austen, some of the recent findings on the molecular biology of mast cell secretory granule proteins and proteoglycans, and the interaction of mast cells with fibroblasts in the presence and absence of interleukin 3(IL-3) are highlighted.     

Propranolol affects stress-induced leukocytosis and cellular adhesion molecule expression

In this study, the impact of the beta-adrenergic antagonist propranolol on resting and acute psychological- and physical-stress-induced circulating leukocyte numbers and the density of cellular adhesion molecules was investigated. In a randomized double-blind crossover design, 45 healthy volunteers performed a 15-min public speaking task and 21 subjects performed a 16-min bicycle exercise after 5 days of ingesting a placebo and after 5 days of ingesting 100 mg/day propranolol. One week of ingesting propranolol modestly elevated the numbers of CD62L+ (P<0.019) but not CD62L- T-lymphocytes. Moreover, propranolol preferentially blunted-psychological stress-induced increases in na?ve T-helper (CD4+CD62L+; P<0.049) and na?ve T-cytotoxic lymphocytes (CD8+CD62L+; P<0.003), as well as activated T-cytotoxic lymphocytes (CD8+CD29+; P<0.005). However, exercise-induced increases in leukocyte numbers were enhanced following propranolol treatment (P<0.04). In contrast to the effect on the numbers of adhesion-molecule-bearing cells, there was only a modest effect of propranolol on stress-induced alterations of the density of CD62L, CD54 and CD11a. In this study, propranolol treatment interfered with the adrenergic regulation of circulating leukocyte numbers by blunting psychological stress effects but enhancing exercise effects. Propranolol affected the cell activation status to a lesser extent, as reflected by the density of adhesion molecules.     

Adenosine deaminase as costimulatory molecule and marker of cellular immunity

Adenosine deaminase (ADA) is an enzyme of purine metabolism which has been the subject of much interest because the congenital defect of this enzyme causes severe combined immunodeficiency syndrome. One of the three isoforms of the enzyme (ecto-ADA) is capable of binding to the glycoprotein CD26 and adenosine receptors A1 and A2B. ADA-CD26 interaction produces a costimulatory signal in the events of T cell activation and secretion of IFN-gamma, TNF-alpha and IL-6. During this activation, the enzyme activity is regulated positively by IL-2 and IL-12 and negatively by IL-4, based on the mechanism of translocation. Diverse studies suggest that seric and plasmatic levels of ADA rise in some diseases caused by microorganisms infecting mainly the macrophages and in hypertensive disorders, which may represent a compensatory mechanism resulting from increased adenosine levels and the release of hormones and inflammatory mediators estimulated by hipoxia.     

Recent advances in cellular immunology: implications for immunity to cancer

Basic immunologists, animal experimenters and clinicians came together earlier this year to discuss insights into, and applications of, cellular immunity to cancer. Major questions critical to the further evaluation and exploitation of the cellular immune response to cancer were explored. It was clear from this conference that there has been a move beyond phenomenology to reductionistic approaches to understanding immune events, raising hopes that the specificity of the T-cell response might be applied to the problem of human cancer.