Inductive effect of Porphyromonas gingivalis fimbriae on differentiation of human monocytic tumor cell line U937

This study used the human monocytic tumor cell line U937 to examine whether Porphyromonas gingivalis fimbriae induce differentiation of monocyte/macro-phage progenitors. When the progenitor cells were incubated with P. gingivalis fimbriaè, the incubation resulted in increased Fc rosette formation and increased CDllb production by the cells. The presence of a protein kinase C inhibitor, H7 or calphostin C, in the medium eliminated the stimulatory effects of P. gingivalis fimbriae on Fc rosette formation. Furthermore, CD11b expression was inhibited by calphostin C. In contrast, HA1004, an inhibitor of cyclic nucleotide-dependent protein kinase, had no effect on P. gingivalis fimbriae-induced Fc rosette formation or CD11b expression. These results demonstrate that P. gingivalis fimbriae are a potent inducer of the differentiation of the monocyte/macrophage tumor cell line U937, most probably via cyclic nucleotide-independent protein kinase C.     

Chemotaxis of human monocytes by synthetic peptides that mimic segments of Porphyromonas gingivalis fimbrial protein

Porphyromonas gingivalis strain 381 fimbriae and their synthetic peptide segments were assessed for migration-stimulating activity on human peripheral blood monocytes by multiwell chemotaxis assay. P. gingivalis 381 fimbrial protein was found to markedly enhance migration of human monocytes. The observed increase in monocyte migration occurred mainly directed toward a positive stimulus (chemotaxis). Furthermore, lipopolysaccharides extracted from P. gingivalis 381 were shown to induce chemotaxis and chemokinesis. It was also revealed that the migration of monocytes was increased by specific synthetic peptide segments, FP381(61–80) and FP381(171–185), that correspond to GKTLAEVKALTTELTAENQE and DANYLTGSLTTFNGA, respectively, based on the ammo acid sequence of the fimbrial subunit protein proposed by Dickinson et al., and the migration stimulation was ascribed to chemotaxis. Furthermore, within the amino acid sequences, the LTXXLTXXN sequence may play an important role in binding the organisms to monocytes and macrophages and in the induction of migration-stimulating activity.     

K88抗原基因研究进展(文献综述)

K88抗原是存在于肠毒性大肠杆菌表面的一种伞毛蛋白质。借伞毛的作用,肠毒性大肠杆菌可以吸附到仔猪小肠上皮细胞粘膜上,并在那里增殖,分泌肠毒素,引起仔猪腹泻、死亡。K88抗原是由约50md的大质粒编码的,通过重组和突变技术,对它们的性质进行了研究。     

针刺督脉穴对血管性痴呆模型大鼠行为及细胞凋亡影响的实验研究

目的:评价针刺督脉穴对血管性痴呆(Vascular dementia,VD)大鼠模型的学习记忆改善情况及可能机制,为针刺治疗血管性痴呆提供理论依据。方法:采用两侧颈总动脉血管阻断加硝普钠降压法复制VD大鼠模型;对VD大鼠模型进行西药(喜得镇)、针刺和电针干预;采用morris水迷宫法观察学习记忆情况;应用免疫组化法测定海马CA1区Bcl-2、Bax蛋白表达及原位末端标记法检测细胞凋亡。结果:(1)morris水迷宫学习记忆能力检测,经过6次训练,与对照组比较,模型组跳台时间延长;与模型组比较,各治疗组跳台时间明显缩短,差异均有统计学意义(P<0.05)。(2)凋亡相关蛋白检测结果显示:与对照组比较,模型组海马组织bcl-2、bax及细胞凋亡明显增高,差异均有统计学意义(P<0.01);与模型组比较,各治疗组海马组织bcl-2水平增高,bax及细胞凋亡水平明显降低,差异均有统计学意义(P<0.01)。结论:(1)各治疗组均可改善VD模型大鼠的认知能力,提高学习记忆成绩。(2)各治疗组均可抑制VD大鼠海马组织细胞凋亡。     

电针督脉穴对血管性痴呆大鼠行为海马氧化应激影响的实验研究

[目的]评价电针督脉穴对血管性痴呆(Vascular dementia,VD)大鼠模型的学习记忆改善情况及可能机制,为治疗血管性痴呆提供理论依据。[方法]采用两侧颈总动脉血管阻断加硝普钠降压法复制VD大鼠模型。对VD大鼠模型进行西药(喜得镇)、针刺和电针干预。采用morris水迷宫法观察学习记忆情况。[结论]①各治疗组均可改善VD模型大鼠的认知能力,提高学习记忆成绩;②与西药组和针刺组比较,电针组能明显提高VD大鼠海马组织SOD活性,降低MDA水平。     

Effects of chemical and surgical lesions on levels of chromatographically identified enkephalin-like peptides in rat hippocampus

The present study quantitates the content of Met- and Leu-enkephalin in the rat hippocampus, and provides information on the localization of the enkephalins within the hippocampal neuronal circuitry. Several enkephalins were identified in rat hippocampus, two of which are shown to be Met- and Leu-enkephalin. The levels of these enkephalins, and of other unidentified enkephalin-related peptides, were not depleted by intrahippocampal colchicine, which destroyed the great majority of the hippocampal granule cells and the associated mossy fiber pathway. Entorhinal cortical lesions ablating the perforant pathway input to the hippocampus also did not significantly lower enkephalin levels in the hippocampus. Unilateral fimbrial transection caused a significant bilateral increase in both Met- and Leu-enkephalin levels. This may result from loss of a stimulatory input to putative enkephalin containing interneurons within the hippocampus. The extents of all lesions were verified histologically in hippocampi used for biochemical analysis. No evidence was seen for the presence of enkephalins in the perforant pathway, nor in nerve fibers in the fimbria/fornix, which provide the other main source of hippocampal efferents. The enkephalins are likely to be intrinsic to the hippocampus, in which neuronal cell bodies containing enkephalin-like immunoreactivity have been extensively reported.     

Distribution and origin of vesicular glutamate transporter 2-immunoreactive fibers in the rat hippocampus

This study examined the distribution of vesicular glutamate transporter 2 (VGLUT2)-immunoreactive neuronal structures in the ipsilateral and contralateral hippocampi of unilateral fimbria/fornix transected, unilateral entorhinal cortex ablated, and intact female and male rats. In the hippocampi of intact animals, the highest density of VGLUT2-positive boutons was observed in the supragranular layer of the dentate gyrus, followed by the CA2 pyramidal and oriens layers, and the stratum lacunosum-moleculare of the CA1 field. This staining pattern was identical both in males and in females. Electron microscopic examination revealed that the immunolabeling was confined to axon terminals forming exclusively asymmetric synaptic contacts. The quantitative analysis of the synaptic targets of VGLUT2-positive terminals showed that in the dentate gyrus, 59% of the synaptic targets were dendritic spines, followed by dendritic shafts (22%) and granule cell somata (19%). In the pyramidal layer of the CA2 field, VGLUT2-immunoreactive boutons contacted mostly dendritic shafts (85%), only some of which (15%) synapsed with spines. The synaptic targets of VGLUT2-positive varicosities were dendritic spines (71%) and shafts (29%) in the stratum lacunosum-moleculare of the CA1 field. The fimbria/fornix transection caused a significant reduction in the density of VGLUT2-positive boutons only in the CA2 field, while entorhinal cortex ablation elicited no change in fiber density in any of the areas analyzed. Furthermore, our latest experiments on colchicine-treated animals revealed a large population of VGLUT2-positive neurons in the hippocampus that may be a possible intrinsic source of hippocampal VGLUT2 boutons. Our results suggest that the most likely sources of VGLUT2-positive boutons in the dentate supragranular layer, the CA2 area, as well as in the stratum lacunosum-moleculare of the CA1 field, might be the mossy cells, the supramammillary area, and the nucleus reuniens thalami, respectively.     

穹窿海马伞损伤对大鼠学习记忆和海马GFAP阳性神经胶质细胞的影响

为探讨穹隆海马伞损伤鼠学习记忆能力与海马胶质纤维酸性蛋白阳性细胞之间的关系 ,切断 SD成年大鼠左侧穹窿海马伞 ,用 Y迷宫和免疫组织化学结合图像分析系统测试大鼠学习记忆能力和海马胶质纤维酸性蛋白阳性细胞的变化状况及它们的相互关系。结果显示 :损伤 2周后 ,损伤组损伤侧海马 CA1 区辐射层和齿状回分子层胶质纤维酸性蛋白阳性细胞的数密度较正常组分别增多 3 0 .2 9%和 3 0 .15 % (都为 P<0 .0 1) ,胞体面积分别增加 16.0 4%和 19.42 % (都为 P<0 .0 1) ,齿状回分子层胶质纤维酸性蛋白阳性细胞体密度增大 19.40 % (P<0 .0 5 )。经相关分析 ,大鼠学习记忆能力与海马 CA1 区胶质纤维酸性蛋白阳性细胞数密度呈负相关 (r=-0 .83 6,P<0 .0 1) ,与齿状回数密度呈负相关 (r=-0 .792 ,P<0 .0 1)。提示海马星形胶质细胞可能参与学习记忆过程     

Regionally specific changes in the hippocampal circuitry accompany progression of cerebrospinal fluid biomarkers in preclinical Alzheimer's disease

Neuropathological and in vivo brain imaging studies agree that the cornu ammonis 1 and subiculum subfields of the hippocampus are most vulnerable to atrophy in the prodromal phases of Alzheimer's disease (AD). However, there has been limited investigation of the structural integrity of the components of the hippocampal circuit, including subfields and extra‐hippocampal white matter structure, in relation to the progression of well‐accepted cerebrospinal fluid (CSF) biomarkers of AD, amyloid‐β 1‐42 (Aβ) and total‐tau (tau). We investigated these relationships in 88 aging asymptomatic individuals with a parental or multiple‐sibling familial history of AD. Apolipoprotein (APOE) ?4 risk allele carriers were identified, and all participants underwent cognitive testing, structural magnetic resonance imaging, and lumbar puncture for CSF assays of tau, phosphorylated‐tau (p‐tau) and Aβ. Individuals with a reduction in CSF Aβ levels (an indicator of amyloid accretion into neuritic plaques) as well as evident tau pathology (believed to be linked to neurodegeneration) exhibited lower subiculum volume, lower fornix microstructural integrity, and a trend towards lower cognitive score than individuals who showed only reduction in CSF Aβ. In contrast, persons with normal levels of tau showed an increase in structural MR markers in relation to declining levels of CSF Aβ. These results suggest that hippocampal subfield volume and extra‐hippocampal white matter microstructure demonstrate a complex pattern where an initial volume increase is followed by decline among asymptomatic individuals who, in some instances, may be a decade or more away from onset of cognitive or functional impairment.