红毛五加多糖对巨噬细胞细胞化学和超微结构的影响

本实验选用中药红毛五加多糖（ＡＧＰＳ）进行小鼠腹腔注射,对腹腔巨噬细胞细胞化学定性、定位、定量进行研究,并观察超微结构的改变,初探作用机理。实验显示了ＡＧＰＳ能使巨噬细胞数量明显增多,体积增大,细胞内糖类,酸性磷酸酶、三磷酸腺苷酶、酸性酯酶和琥珀酸脱氢酶活性显著增强。用显微分光光度计进行单细胞化学成份定量测定,实验组与对照组有显著差异,提示ＡＧＰＳ的扶正固本作用十分明显。扫描电镜显示表面微绒毛增多、增粗、增长,交错重叠或成簇、密集杂乱。透射电镜可见胞质内糖原颗粒增多、线粒体丰富、溶酶体增加,揭示了巨噬细胞活化的形态学基础。     

红毛五加多糖不同组分对小鼠腹腔巨噬细胞免疫功能的研究

本文研究红毛五加多糖不同组分(AHP-I、AHP-II、AHP-III)对小鼠腹腔巨噬细胞免疫调节功能的影响,为进一步阐明红毛五加多糖对小鼠免疫调节作用机制奠定基础。采用不同浓度的3种多糖组分作用于小鼠腹腔巨噬细胞,测定其对巨噬细胞吞噬中性红、释放NO能力、分泌IL-6、TNF-α、IL-1β水平的影响。最后结果是红毛五加多糖的3种不同组分对小鼠免疫细胞有不同的刺激能力。其中,AHP-II可极其显著地增强吞噬细胞的吞噬功能,促进其合成NO,促进巨噬细胞细胞因子的分泌。因此红毛五加多糖能激活小鼠腹腔巨噬细胞,其中,AHP-II是最重要的作用组分。     

红毛五加多糖单一组分AHP-Ⅲ对巨噬细胞的免疫调节作用及其机制

探讨红毛五加多糖(Acanthopanax giraldii Hams polysaccharide)单一组分AHP-Ⅲ(Acanthopanax giraldii Hams polysaccharideⅢ)对小鼠巨噬细胞RAW 264.7的激活作用及机制。不同浓度AHP-Ⅲ作用RAW 264.7细胞,中性红试验检测细胞吞噬能力;ELISA和Griess法检测其IL-6、TNF-α和NO的释放量;RT-qPCR检测iNOS、TNF-α和IL-6 mRNA相对表达水平;Western blot检测NF-κB信号通路相关蛋白磷酸化水平。在实验浓度范围内,AHP-Ⅲ可显著增强RAW 264.7细胞的吞噬能力(P<0.05);促进RAW 264.7分泌NO、TNF-α和IL-6(P<0.05或P<0.001);并显著增加RAW 264.7细胞中IL-6、TNF-α和iNOS mRNA的表达量,呈剂量依赖性;Western blot结果表明,AHP-Ⅲ作用RAW 264.7细胞后,NF-κB中的p65、IKKβ、IκBα磷酸化水平明显升高。结果显示红毛五加多糖AHP-Ⅲ对小鼠巨噬细胞RAW 264.7具有显著激活作用。     

红毛五加多糖AHP-II对THP-1源巨噬细胞中酶活性的影响

本研究检测红毛五加多糖AHP-II对THP-1巨噬细胞内多种酶活性的影响。通过PMA诱导THP-1成为巨噬细胞,用不同浓度的AHP-II与巨噬细胞共孵育48 h后,测定超氧化物歧化酶(SOD)、琥珀酸脱氢酶(SDH)、酸性磷酸酶(ACP)、ATP酶的活性及溶菌酶(LZM)含量变化。结果显示AHP-II能显著增强细胞内的SOD、SDH、ACP和ATP酶的活性及LZM的含量。     

五加皮及其混乱品种的药理作用研究

本文对刺五加、细柱五加、红毛五加、香加皮的醇提物及红毛五加水提物五种药液的药理作用进行了比较研究。结果如下：（１）分组腹腔注射五种药液对巴豆油引起的小鼠耳部炎症均有显著的抑制作用,其中以红毛五加水提物的抗炎作用最强。（２）灌胃给五种药液只有红毛五加水提物和刺五加醇提物能明显延长小鼠游泳时间。（３）对环磷酰胺所致白细胞数减少的小鼠分组灌胃五种药液,结果表明红毛五加水提物、刺五加醇提物及细柱五加醇提物均有明显的升白作用。（４）在研究五种药液影响巴比妥钠诱导小鼠睡眠的实验中,结果显示灌胃刺五加醇提物能明显延长小鼠的睡眠时间,香加皮和红毛五抓醇提物则明显缩短小鼠的睡眠时间,细住五加醇提物和红毛五加水提物对小鼠睡眠时间无影响。     

红毛五加多糖对大鼠肝细胞免疫损伤的保护作用及其机制

红毛五加属于五加科植物,而五加科植物大多具有调节免疫力的双向调节作用,红毛五加多糖是从中药红毛五加中提取的单一组分,目前关于红毛五加多糖的抑炎作用还少有报道。为了探究红毛五加多糖AHP-Ⅱ对LPS导致的大鼠肝细胞免疫损伤的保护作用及其作用机制,该研究将实验分为空白组、模型组(LPS,40μg·mL^-1)和AHP-Ⅱ低、中、高剂量组(25,50,100μg·mL^-1)五组,以LPS(40μg·mL^-1)来制备大鼠肝细胞免疫损伤模型,先用ELISA方法检测细胞分泌TNF-α的水平及流式检测ROS的含量,来探究AHP-Ⅱ不同剂量对炎症因子的抑制作用,再用western方法检测P-JNK2的蛋白水平来进一步探究AHP-Ⅱ的抑制作用机制。结果表明:低、中、高剂量组的AHP-Ⅱ均可使肝细胞损伤后的TNF-α含量下降。同时,AHP-Ⅱ中、高剂量组均可使损伤后的肝细胞ROS的分泌量下降,且AHP-Ⅱ高剂量组抑制ROS的作用最强。在加入AHP-Ⅱ后,JNK2蛋白的磷酸化水平呈剂量依赖性降低,AHP-Ⅱ高剂量组抑制作用最强。这说明红毛五加多糖AHP-Ⅱ可以通过降低P-JNK2的蛋白含量来抑制炎症因子TNF-α及ROS的水平,以发挥免疫保护作用。     

红毛五加茎皮多糖对体外培养人白血病粒细胞生物学效应的研究

本文采用体外培养方法就红毛五加茎皮多糖对癌细胞生物学效应及其抗癌机制进行了初探。实验结果证明,红毛五加茎皮多糖具有良好的抗癌效果,能使体外培养的人白血病粒细胞形态明显改变,癌细胞生长受抑制,细胞生长曲线下降,细胞死亡率上升,流式细胞分光光度计测定分析,提示癌细胞合成ＤＮＡ的前期受到抑制,阻断ＤＮＡ的合成。     

环境污染物对巨噬细胞的影响及生物监测意义

研究环境污染物亚硫酸盐和无机汞对小鼠腹腔巨噬细胞的影响,探讨巨噬细胞作为生物监测指示物的意义。实验取小鼠腹腔巨噬细胞分别经Na_2SO_3和HgCl_2体外培养,光镜和电镜下观察细胞形态学改变,检测其NO产量,还原MTT能力和吞噬功能。结果显示,小鼠腹腔巨噬细胞染毒后,细胞形态均发生显著改变;NO浓度明显降低,还原MTT能力受抑制,吞噬功能明显减弱(p<0.05或p<0.01)。高浓度(10~(-4)mol/L)HgCl_2细胞毒性作用显著,可致巨噬细胞坏死。实验表明,Na_2SO_3和HgCl_2对小鼠腹腔巨噬细胞具有明显损伤作用,进而直接影响巨噬细胞的非特异性防御功能。实验提示巨噬细胞可作为生物监测指示物,应用于环境污染的生物监测。     

成纤维细胞生长因子-7在巨噬细胞感染结核分枝杆菌中的免疫机制初步研究

巨噬细胞分泌的纤维细胞生长因子-7(fibroblast growth factor-7,FGF-7)具有一定的细胞修复作用及抗炎症作用。通过PCR技术、Western-blot及ELISA实验研究分析FGF-7在巨噬细胞感染结核分枝杆菌(Mycobacterium tuberculosis,M.avium)后的分子免疫机制。研究发现fgf-7基因在结核病患者外周血单个核细胞中表达增强,并且U973巨噬细胞在感染M.avium后,其fgf-7基因与FGF-7蛋白亦表达增强,同时U973巨噬细胞上清中的细胞因子TNF-α与IFN-γ分泌量显著增加。实验结果表明巨噬细胞受M.avium感染后,M.avium可增强巨噬细胞fgf-7基因及其蛋白质的表达,并促进细胞因子TNF-α与IFN-γ的分泌;提示FGF-7可能与TNF-α、IFN-γ等共同引起炎症反应从而参与对M.avium的抑制或杀伤作用,并修复损伤的巨噬细胞。     

转移因子对小鼠腹腔巨噬细胞吞噬功能的影响和E玫瑰花形成的作用

本文报道了转移因子对小鼠腹腔巨噬细胞吞噬功能的影响和对脾细胞E玫瑰花形成的作用。转移因子为本单位从健康猪脾细胞提取的针剂,含多核苷酸和多肽等低分子生物活性物质,每支含量为3×10~3个脾细胞提取物,每天一次0.5ml剂量注入小鼠体内,连续5次后取动物腹腔巨噬细胞和脾细胞悬液,测定其吞噬功能并观察E玫瑰花形成作用。结果表明,转移因子对小鼠腹腔巨噬细胞吞噬的百分率和吞噬指数与对照组比有明显差异(P<0.01),对小鼠脾细胞E玫瑰花形成作用与对照组比差异也极显著(P<0.01)。从而看出,转移因子能使小鼠腹腔巨噬细胞吞噬功能增强,亦能使特异的玫瑰花形成细胞中T淋巴细胞增多,增强了机体的免疫功能。     

党参对冠心病心绞痛患者的血液细胞及对小鼠心肌作用的定量细胞化学观察

本文应用细胞化学和定量细胞化学技术,对冠心病心气虚病人服用党参前后外周血细胞中的糖原及琥珀酸脱氢酶（ＳＤＨ）的含量和活性,以及党参对小鼠心肌中糖原、ＳＤＨ、乳酸脱氢酶（ＬＤＨ）的影响进行了分析研究。结果发现,党参可明显提高冠心病人外周血细胞中糖原和ＳＤＨ的含量和活性;同时动物实验亦证实,灌服党参液的小鼠心肌中糖原、ＳＤＨ、ＬＤＨ的含量和活性亦明显高于生理盐水组。这说明党参可改善冠心病人的心肌代谢,对冠心病的治疗是十分有利的。     

Plasmalogen synthesis is regulated via alkyl-dihydroxyacetonephosphate-synthase by amyloid precursor protein processing and is affected in Alzheimer's disease

Lipids play an important role as risk or protective factors in Alzheimer's disease, which is characterized by amyloid plaques composed of aggregated amyloid-beta. Plasmalogens are major brain lipids and controversially discussed to be altered in Alzheimer's disease (AD) and whether changes in plasmalogens are cause or consequence of AD pathology. Here, we reveal a new physiological function of the amyloid precursor protein (APP) in plasmalogen metabolism. The APP intracellular domain was found in vivo and in vitro to increase the expression of the alkyl-dihydroxyacetonephosphate-synthase (AGPS), a rate limiting enzyme in plasmalogen synthesis. Alterations in APP dependent changes of AGPS expression result in reduced protein and plasmalogen levels. Under the pathological situation of AD, increased amyloid-beta level lead to increased reactive oxidative species production, reduced AGPS protein and plasmalogen level. Accordingly, phosphatidylethanol plasmalogen was decreased in the frontal cortex of AD compared to age matched controls. Our findings elucidate that plasmalogens are decreased as a consequence of AD and regulated by APP processing under physiological conditions.     

Medical monitoring during the NASA Artificial Gravity-Bed Rest Pilot Study

The NASA artificial gravity-bed rest pilot study (AGPS) was designed to investigate the efficacy of daily exposure to a +Gz acceleration gradient for counteracting the physiologic decrements induced by prolonged bed rest. Test subjects were continuously monitored by a physician for signs and symptoms of pre-syncope, motion sickness, and arrhythmias while on the centrifuge. In this article, we have summarized the medical monitoring observations that were made during the AGPS and included an assessment of the relative usefulness of the information provided by the various monitoring tools in making a decision to terminate a centrifuge spin.     

Immune-mediated interactions during macrophage development in non-Hodgkin's lymphoma.

As part of an investigation of mononuclear phagocytes in malignant lymphoma, measurement of immune-mediated erythrophagocytosis and rosette formation was carried out on cells grown in suspension culture at the monocyte (Day 0) and macrophage (Day 6) stages; the culture medium contained autologous serum. Cells were derived from 10 patients with untreated non-Hodgkin's lymphoma (NHL) and from 12 normal individuals. The results were subjected to Analysis of Variance and demonstrated a significant difference between the two groups with respect to erythrophagocytosis but not to rosette formation. In the NHL group, the proportion of erythrophagocytic cells showed no significant increase between the monocyte and macrophage stages (0.07 to 0.09), in contrast to the marked increase seen in the normal group (0.09 to 0.24). In a pilot investigation to examine the possible role of factors in the serum, cells derived from the NHL patients were cultured with serum from healthy donors; they showed no significant difference in the immune-mediated functions from those grown in autologous serum. Overall, the results provide further quantitative evidence of defective macrophage maturation in NHL, presumably reflecting the compromise of host defence mechanisms.     

Differential regulation of colony stimulating factor 1 and macrophage migration inhibitory factor expression by inflammatory cytokines in term human decidua: implications for macrophage trafficking at the fetal-maternal interface

Macrophages are a major component of the leukocyte population of human pregnant endometrium. Although several crucial functions have been ascribed to these cells, the mechanisms underlying macrophage trafficking in the placental bed are poorly understood. The aim of this study was to evaluate the in vivo expression of two potentially antagonistic macrophage-targeting chemokines, colony stimulating factor 1 (CSF1, also known as M-CSF) and macrophage migration inhibitory factor (MIF), in term decidua, and to examine the effects of the inflammatory cytokines tumor necrosis factor (TNF, also known as TNF alpha) and interleukin 1beta (IL1B) on CSF1 and MIF expression in cultured decidual cells. The expression of CSF1 and MIF in term decidua was evaluated by immunohistochemistry. Cultured decidual cells were primed with estradiol (E2) or with E2+medroxyprogesterone acetate (MPA), and then incubated with corresponding steroid(s) with or without TNF or IL1B. The levels of CSF1 and MIF protein and mRNA were assessed by ELISA and quantitative RT-PCR, respectively. Immunostaining for CSF1 and MIF was observed in term decidua. The levels of secreted CSF1 and MIF were similarly unchanged whether the decidual cells were incubated with E2 or with E2+MPA. The CSF1 levels significantly increased in cultures exposed to E2 or E2+MPA plus TNF or IL1B. In contrast, the MIF levels in TNF- and IL1B-treated cells were not changed significantly from the control cultures. The ELISA data were confirmed by quantitative RT-PCR analysis. These results indicate that CSF1 and MIF are involved in regulating macrophage trafficking at the fetal-maternal interface, and suggest a mechanism by which inflammatory cytokines influence pregnancy by regulating decidual macrophage infiltration.     

鲇鱼成鱼和幼鱼中含色素的巨噬细胞集结的诱导发生

通过腹腔注射不同剂量的牛血清白蛋白（ＢＳＡ）或墨汁以刺激巨噬细胞活动,研究了鲇鱼成鱼和幼鱼头肾、肾、脾和肝中含色素的巨噬细胞集结（ＰＭＡ）的发生。鲇鱼淋巴样组织中存在巨噬细胞的不均一性,可分网状／纤维状巨噬细胞,梭状巨噬细胞,圆形红色巨噬细胞,圆形黄红色巨噬细胞和含色素的巨噬细胞。注射ＢＳＡ或墨汁后,头肾、肾,脾和肝中ＰＭＡ和圆形巨噬细胞的数量最终均有不同程度的增加。通过诱导发生实验,表明含色素的     

脑缺血再灌流诱导的巨噬细胞增加的组织化学研究

用组织化学方法显示非特异性酯酶,观察了大鼠脑缺血再灌流脑组织巨噬细胞数量的变化。结果显示,大鼠脑缺血１ｈ再灌流２ｈ巨噬细胞数量明显高于正常对照组（Ｐ＜０．０５）,再灌流１６ｈ,巨噬细胞数量最多。缺血侧皮质区与基底节区比较,后者巨噬细胞计数明显高于前者（Ｐ＜０．０５）。结果提示,大鼠脑缺血再灌流与脑组织巨噬细胞数量增加有关