精巢间质细胞雄激素合成及其调节的研究进展

本文综述了近年来精巢间质细胞雄激素的合成及其分泌调节的研究进展。间质细胞内的雄激素合成的限速步骤是胆固醇转化为孕烯醇酮时的胆固醇跨线粒体膜转运。在此转运过程中，PBR可能是作为依赖于配体的通道蛋白，对胆固醇分子进行跨膜转移；StAR则通过解离线粒体膜与胆固醇分子的吸附作用，加速了胆固醇分子的转运。雄激素的合成还受垂体、支持细胞、巨噬细胞和其自身分泌激素和细胞因子的调控。同时对今后研究的方向做了总结和展望。     

Scavenger receptor family proteins: roles for atherosclerosis, host defence and disorders of the central nervous system

In this review, we summarize the structure and function of the scavenger receptor family of proteins including class A (type I and II macrophage scavenger receptors, MARCO), class B (CD36, scavenger receptor class BI), mucinlike (CD68/macrosialin, dSR-CI) and endothelial (LOX-1) receptors. Two motifs have been identified as ligand-binding domains a charged collagen structure of type I and II receptors, and an immunodominant domain of CD36. These structures can recognize a wide range of negatively charged macromolecules, including oxidized low-density lipoproteins, damaged or apoptotic cells, and pathogenic microorganisms. After binding, these ligands can be either internalized by endocytosis or phagocytosis, or remain at the cell surface and mediate adhesion or lipid transfer through caveolae. Under physiological conditions, scavenger receptors serve to scavenge or clean up cellular debris and other related materials, and they play a role in host defence. In pathological states, they mediate the recruitment, activation and transformation of macrophages and other cells which may be related to the development of atherosclerosis and to disorders caused by the accumulation of denatured materials, such as Alzheimer's disease. Received 17 September 1997; received after revision 16 March 1998; accepted 17 March 1998     

氯屈膦酸二钠-超顺磁性氧化铁脂质体减轻重症急性胰腺炎肾损伤

研究目的：探讨氯属膦酸二钠-超顺磁性氧化铁（SPIO）脂质体对重症急性胰腺炎（SAP）肾损伤的保护作用。创新要点：围绕SAP并发多器官损伤这一核心问题,联系巨噬细胞在SAP发病过程中的作用,使用纳米脂质体携带氯屈膦酸二钠及SPIO,以及利用自体巨噬细胞对SAP时多器官损伤的定性靶向性以及磁性纳米颗粒的超顺磁性,应用磁共振成像（MRI）对SAP并发多器官损伤进行早期诊断。结合使用氯屈膦酸二钠,使其促进巨噬细胞的凋亡,减少其在急性胰腺炎早期产生炎症介质,阻止全身性炎症反应的进程,从而实现对多器官损伤的保护作用。研究方法：采用胰腺被膜下均匀注射5％牛磺胆酸钠制作SAP模型。SD大鼠48只,随机分为对照组（C组）、空白SPIO脂质休组（P组）和氯屈膦酸二钠＋SPIO脂质体组（T组）。P组和T组大鼠制作SAP模型。制模2h和6h后取肠系膜上静脉血液,检测各组大鼠血清中淀粉酶、尿素氮、血肌酐和肿瘤坏死因子-α的含量,观察胰腺及肾组织的病理学变化及进行病理评分,通过检测肾组织的TUNEL染色及CD68表达研究氯属膦酸二钠-超顺磁性氧化铁脂质体对肾组织巨噬细胞凋亡的影响并进行MRI诊断。重要结论：氯屈膦酸二钠-超顺磁性氧化铁脂质体可选择性清除单核／巨噬细胞,减少炎症介质释放,对SAP大鼠胰腺及肾损伤有保护作用。SPIO可作为MRI示踪。     

绞股蓝多糖的抗肿瘤作用及其机制研究

本研究通过建立小鼠移植瘤模型,采用荷瘤小鼠抑瘤率检测绞股蓝多糖对小鼠肉瘤S180的体内抗肿瘤作用;采用MTT法检测绞股蓝多糖对体外培养的肿瘤细胞增殖的抑制作用。此外,采用比色法测定了绞股蓝多糖对巨噬细胞吞噬率和产生细胞因子NO的影响;采用ELISA法测定了绞股蓝多糖对巨噬细胞产生IL-1β和TNF-α的影响。 绞股蓝多糖可明显抑制移植性动物肿瘤S180的生长,并呈明显的剂量依赖关系;经绞股蓝多糖刺激后,小鼠巨噬细胞对中性红的吞噬功能明显的增强,并能显著刺激巨噬细胞分泌NO、TNF-α和IL-1β。本研究为绞股蓝多糖的进一步开发提供了实验数据。     

雪莲多糖对小鼠脾虚模型腹腔巨噬细胞吞噬功能的影响

根据中医饮食失节,过食肥甘,饥饿等均可伤元气、损脾胃的理论,本次试验以莲花白、猪脂为主饲喂小鼠,复制成脾阳虚模型,将其分为Ⅰ、Ⅱ、Ⅲ组,Ⅰ组小鼠每日灌服雪莲多糖液0.5ml(含多糖25mg)/只,Ⅱ、Ⅲ组每日分别灌服四君子汤1ml(含生药1g)/只和生理盐水0.5ml/只,另以正常小鼠作对照(Ⅳ组),每日灌服生理盐水0.5ml/只,均各连服7天。在停药前两天,全部小鼠均以含可溶性淀粉5％为溶液1ml/只作腹腔注射,停药后的翌日,检测各组腹腔巨噬细胞对鸡红细胞的吞噬指数和吞噬百分率。结果Ⅰ组均值分别为0.457±0.0655,40.0±7.75％;Ⅱ组0.260±0.0498,21.6±4.81％;Ⅲ组0.220±0.0444、16.8±4.29％;Ⅳ组0.244±0.0532,20.1±4.99％,Ⅰ组两项指标明显高于其余各组,差异均极显著(p<0.001),表明雪莲多糖对脾阳虚小鼠腹腔巨噬细胞的吞噬功能有明显的增强作用。     

Regulation of macrophage activation

IFN- rapidly primes the macrophage via JAK1/2-STAT1 pathway so that it can subsequently undergo a slower classical type 1 activation upon exposure to T helper (Th)1 cytokines such as IFN or other activators, including tumor necrosis factor and lipopolysaccharide, e.g. in intracellular killing of phagocytosed Mycobacterium tuberculosis. If instead it is driven by Th2 cytokines interleukin (IL)-4 and IL-13, it undergoes alternate type 2 activation, which enhances endocytotic antigen uptake and presentation, mast cell and eosinophil involvement and type 2 granuloma formation, e.g. in response to parasitic and extracellular pathogens. Particle-induced macrophage activation was shown to differ from classical and alternate activation, showing in DNA microarray experiments (complete linkage/ Euclidean distance metric analysis) upregulation of nonsecreted structural/signaling molecules and lack of secreted proin-flammatory cyto- and chemokines. The switch-off (deactivation) of already activated macrophages is an active, controlled process in which IL-10 and corticosteroids play important roles and to which15dPGJ2, PGA1/2 and vasoactive intestinal peptide often contribute.Received 16 January 2003; received after revision 14 March 2003; accepted 2 April 2003     

绞股蓝多糖的抗肿瘤作用及其机制研究

通过建立小鼠移植瘤模型,采用荷瘤小鼠抑瘤率检测绞股蓝多糖对小鼠肉瘤S180的体内抗肿瘤作用;采用MTT法检测绞股蓝多糖对体外培养的肿瘤细胞增殖的抑制作用.此外,采用比色法测定了绞股蓝多糖对巨噬细胞吞噬率和产生细胞因子NO的影响;采用ELISA法测定了绞股蓝多糖对巨噬细胞产生IL-1β和TNF-α的影响. 绞股蓝多糖可明显抑制移植性动物肿瘤S180的生长,并呈明显的剂量依赖关系;经绞股蓝多糖刺激后,小鼠巨噬细胞对中性红的吞噬功能明显的增强,并能显著刺激巨噬细胞分泌NO、TNF-α和IL-1β.为绞股蓝多糖的进一步开发提供了实验数据.     

香菇发酵营养液的免疫调节作用观察

研究表明,香菇菌株经液体培养提取的香菇营养液,具有可增加小鼠耳肿胀度,其中30ml/kg剂量达到显著水平(P<0.01),且香菇营养液具显著促进巨噬细胞吞噬功能的作用,表明具有较强的免疫功能。     

巨噬细胞移动抑制因子在宫颈癌组织中的表达及临床意义

目的探讨巨噬细胞移动抑制因子（MIF）在宫颈癌组织中的表达,评价其在宫颈癌发生、发展中的作用。方法采用免疫组化SP法检测42例宫颈癌组织及20例正常宫颈组织中MIF的表达。结果MIF在宫颈癌中的阳性表达率明显高于正常宫颈组织（P〈0．05）;MIF表达与宫颈癌的分化程度、临床分期及淋巴结转移密切相关（P〈0．05）,与病理类型及肿瘤直径无关联性（P〉0．05）。结论MIF可能在宫颈癌的发生及进展中起着重要的作用。     

Macrophages derived from bone marrow modulate differentiation of myeloid dendritic cells

Dendritic cells (DC) are specialized antigen-presenting cells. Bone marrow monocytes have been widely used to generate murine myeloid DC. We found that mouse macrophages derived from bone marrow CD11b⁺ monocytes influenced the differentiation of these precursors into DC. Modulation of differentiation was demonstrated by the down-regulation of CD11c, CD40, and CD86 expression and by IL-12 production. DC differentiated in the presence of conditioned medium from bone marrow-derived macrophage culture (MCM) had impaired ability to stimulate proliferation of, and IFN- γ production by, allogeneic CD4⁺ T cells. This inhibition of DC differentiation was mainly mediated by secretory products from macrophages but not by cell-cell contact. MCM contained higher concentrations of macrophage-colony-stimulating factor (M-CSF), IL-10, and TGF- β1, whereas IL-6 remained unchanged compared with conditioned medium from fresh monocytes. M-CSF may be the major mediator in MCM inhibiting DC differentiation. This study demonstrates an important influence of bone marrow-derived macrophages on DC precursors during DC differentiation. Received 12 September 2006; received after revision 20 October 2006; accepted 13 November 2006