壳寡糖对荷瘤鼠肿瘤细胞凋亡的影响

目的 探讨壳寡糖诱导肿瘤细胞凋亡机制,为壳寡糖开发应用提供实验依据.方法 选择小鼠体内注射的方法 将壳寡糖注入荷瘤小鼠体内,观察肿瘤生长情况,计算抑瘤率,流式细胞仪测定细胞凋亡率,电镜观察肿瘤细胞超微结构.原位杂交法检测Survivin mRNA表达.结果 壳寡糖抑瘤率为42.03%,流式细胞仪检测壳寡糖凋亡率20.68%,与模型组比较,差异有统计学意义.壳寡糖组镜下可见瘤细胞以凋亡变化为主,壳寡糖下调肿瘤细胞Survivin mRNA表达,与模型组比较,差异具有统计学意义.结论 壳寡糖可诱导肿瘤细胞凋亡,其机制可能与下凋Survivin mRNA表达密切相关.     

蝉拟青霉多糖对大鼠免疫功能的调节作用

目的：探讨不同剂量蝉拟青霉多糖对大鼠免疫功能的调节作用。方法： 每天给大鼠称重，并按所称大鼠体重，以50、100、200 mg/kg的蝉拟青霉多糖(PCPS)剂量在大鼠后背部皮下注射给药半个月。处死大鼠后称脾和胸腺湿重，并计算其湿重指数；计数大鼠外周血白细胞(WBC)数；以双试剂终点法测定酸性磷酸酶(ACP)、速率法测定乳酸脱氢酶(LDH)及测定精氨酸酶(arginase)等活力；进行大鼠肺泡巨噬细胞(AM)中性红吞噬试验。结果：PCPS组大鼠脾脏、胸腺湿重指数及白细胞计数显著高于对照组；PCPS组大鼠肝、肾、脾、胸腺内ACP、LDH活力显著升高，AM吞噬功能显著增强，AM内ACP、LDH、arginase活力显著提高(P＜0.01，P＜0.05)。结论： 不同浓度蝉拟青霉多糖能提高大鼠外周血WBC数，激活肺泡巨噬细胞，并具有剂量依赖性。     

壳寡糖对新西兰兔骨折愈合的影响

目的：观察甲壳质衍生物一壳寡糖在新西兰兔骨折愈合中的作用及其作用机制。方法：用新西兰兔制备右桡骨中段3mm骨缺损模型后．每日灌胃给予壳寡糖0．28g／kg。术后9、17、30、42 d 4个时间段,X-线片、地衣红染色观察骨折愈合情况;免疫组织化学方法观察转化生长因子β1(TGF—β1)蛋白的表达,并用VIDAS图像分析系统进行半定量分析。结果：实验组在各时间段的骨折愈合情况均显著好于对照组;在9、17d时,实验组骨折端中TGP-β1的表达均较对照组明显增高。结论：壳寡糖能促进兔骨折的愈合,其机制可能与其促进胶原形成、提高骨折愈合早期TGF-β1的表达有关。     

壳寡糖抑制肿瘤作用的实验研究

目的：通过建立H22肝癌荷瘤鼠作为实验动物模型，研究壳寡糖对肿瘤抑制作用的影响。方法：选择小鼠体内注射的方法，将不同浓度壳寡糖注入荷瘤小鼠体内，观察肿瘤生长情况，对其进行免疫功能的测定；同时通过MTT比色法观察壳寡糖对LH-7人肺癌细胞的体外生长抑制作用。结果：壳寡糖对肿瘤的生长有抑制作用；壳寡糖可提高荷瘤小鼠血清的IL-2和IFN-γ含量，增加荷瘤小鼠免疫器官脾脏和胸腺重量；显微镜观察肿瘤组织出现坏死；壳寡糖对LH-7细胞生长有抑制作用，抑瘤率与浓度有关，与时间无关；透射电镜显示细胞有凋亡趋势。结论：壳寡糖可抑制肿瘤生长，提高机体免疫功能；同时壳寡糖可能诱导LH-7肿瘤细胞凋亡。     

玉屏风散对免疫抑制小鼠免疫功能的调节作用

玉屏风散、出自元·朱丹溪的《丹溪心法》,由黄芪、白术和防风等组成,具有益气固表、扶正止汗、祛风御风等功效。现代研究表明,方中的黄芪和白术对机体的部分免疫指标具有促进作用。我们观察了玉屏风散对免疫抑制小鼠免疫功能的影响。1 材料和方法1．1 材料玉屏风水煎液：按《中华人民共和国药典》的标准取黄芪、防风和白术常规煎煮3次,去渣、混合、浓缩配成1 kg/L的玉屏风水煎液。昆明种小白鼠,6-8 wk, 体质量(20±2)g,雌雄兼用;健康家兔、健康来亨公鸡和健康豚鼠均购自本校实验动物中心。RPMI1640培养基、胎牛血清(FCS)为G…     

槲皮素对小鼠动情周期及免疫功能的调节作用

目的:研究槲皮素对小鼠动情周期的影响及其免疫效应,并探讨其作用机制。方法:对小鼠连续7天灌胃给予浓度为2.5 mg/ml的槲皮素药液0.5 ml/(天.只),通过阴道脱落细胞学检查法判断未经产雌鼠所处的动情周期,并利用MTT法检测脾淋巴细胞转化率、α-醋酸萘酯酶法检测T淋巴细胞数量、碳廓清实验检测吞噬细胞活性、定量溶血分光光度法检测IgM抗体生成量。结果:槲皮素显著延长了小鼠的动情周期,并可以明显增加淋巴细胞转化率和T淋巴细胞数目、增强小鼠巨噬细胞的吞噬活性和IgM抗体的生成。结论:槲皮素对小鼠子宫内膜的周期性变化造成了影响,对小鼠机体起到了免疫增强作用。     

壳寡糖对子宫内膜癌细胞增殖迁移的影响及可能分子机制

目的 探讨壳寡糖对子宫内膜癌细胞增殖迁移的影响及可能分子机制.方法 将不同浓度的壳寡糖作用于子宫内膜癌HEC-1B细胞,通过CCK-8检测细胞的增殖情况;划痕实验检测细胞迁移情况;Western blot检测E-cadherin、Snail、MMP2和MMP9及AMPK/mTOR的蛋白表达.结果 1.25mg/ml的壳...     

纳洛酮对人体短时剧烈运动中机体免疫功能的影响

本文就纳洛酮对击剑运动员短时间剧烈运动前后机体免疫功能的影响进行了初步探讨,结果表明:运动前静脉注射纳洛酮后跑步4000米,外周血T细胞亚群的变化表现为CD_8~+细胞亚群百分率升高,CD_4~+/CD_8~+比值下降;运动后外周血白细胞诱生干扰素的能力显著高于运动前,P值<0.01。运动后NK细胞活性及白细胞吞噬百分率有下降的趋势,但吞噬指数显著增高。纳洛酮对外周血白细胞诱生干扰素的能力、NK细胞活性及白细胞吞噬功能均未见有明显影响。     

玉米多糖对小鼠机体免疫功能的影响

玉米(Zea mays L.)为一年生禾本科草本植物。玉米营养丰富,除蛋白质、脂肪和粗纤维外,还含有多种活性多糖,已有研究表明,玉米多糖具有抗便     

氨基葡萄糖和壳寡糖对去势大鼠血液生化指标的影响

目的:探讨氨基葡萄糖(GLC)和壳寡糖(COS)对去势大鼠动物模型血液生化指标的影响,进一步研究其抗骨质疏松的作用,以期为临床骨质疏松的防治和新药、功能性食品开发提供理论和实验依据。方法:通过切除3月龄雌性大鼠双侧卵巢复制绝经骨质疏松动物模型,每日分别给予不同剂量的氨基葡萄糖和壳寡糖,心脏取血观察血清生化指标的变化。结果:模型组碱性磷酸酶(ALP)、抗酒石酸酸性磷酸酶(TRAP)、甘油三酯(TG)、胆固醇(CHO)、低密度脂蛋白(LDL)、肌酐(Cr)都明显升高,氨基葡萄糖和壳寡糖中剂量(0.25g/kg)能明显降低上述6个指标的水平(P<0.05)。结论:氨基葡萄糖和壳寡糖对去势大鼠过高的骨转换有明显的抑制作用,并能提高骨再建能力,对去卵巢致骨质疏松有明显的对抗作用。     

Modulation of asthma by endotoxin

Asthma is a common inflammatory disease triggered by both allergic and non‐allergic stimuli. The most common risk factor in the development of asthma is induction of IgE against indoor allergens and imbalance in the T‐helper type 1 (Th1) and Th2 with skewing towards Th2 response. Interplay of genetic and environmental factors is involved in induction and propagation of asthma. Endotoxin is a common environmental pollutant and elicits a Th1 response. The amount of endotoxin varies with several factors but of significant interest has been the role of pets. Endotoxin not only protects against the development of asthma but also enhances an already established inflammation. The difference of outcomes is likely not only due to the time and dose of exposure but also as we discuss the variable interaction of genes with environment. We focus on studies since 2001 that have explored the role of endotoxin in asthma and the gene–environment interactions of the endotoxin effect. Cite this as: V. Doreswamy andD. B. Peden, Clinical & Experimental Allergy, 2011 (41) 9–19.     

Modulation of leukotaxis by ibuprofen

The purpose of this study was to evaluate the rabbit anterior eye chamber as a quantitative measure of leukotaxis using⁵¹Cr-labeled homologous leukocytes and then to determine the effects of ibuprofen onN-formyl-methionyl-leucyl-phenylalanine (FMLP) -induced leukotaxis. Leukocyte accumulation was assessed at various intervals (0–24 h) after instillation of FMLP (10^–4 M, 40l) and at various doses (FMLP 10^–6–10^–4 M). New Zealand white rabbits (2.6–3.0 kg) were treated with ibuprofen for three days with the following regimens: 8.0, 17.5, 35.0, 70.0 mg/kg/day. Leukocyte quantitation was determined using a direct cell count and recovery of⁵¹Cr-labeled leukocytes from anterior eye chamber aspirations 3 h after their injection into the systemic circulation. FMLP induced a dose-dependent accumulation of leukocytes. Leukocyte influx into the anterior eye chamber increased between 2 and 4 h after FMLP instillation, peaking between 4 and 6 h, then resolving after 8 h. Ibuprofen inhibited leukocyte accumulation into the anterior eye chamber in a dose dependent fashion with a maximum (90.0±1.4%, X±SEM) inhibition with 70 mg/kg/day and an ID₅₀ of 8 mg/kg/day. In conclusion, the anterior eye chamber FMLP-stimulated leukotaxis assay is useful to evaluate the role of pharmacologie agents. Here, ibuprofen was found to inhibit leukotaxis in a dose-dependent manner.This project was supported in part by NIH grant HD-19002 and an award from the USC Faculty Research and Innovation Fund.     

Modulation of TRPs by PIPs

The TRP superfamily of cation channels encompasses 28 mammalian members related to the product of the Drosophila trp (transient receptor potential) gene. TRP channels have a widespread distribution in many cell types and organs and gate in response to a broad variety of physical and chemical stimuli; as such, they can be considered as ubiquitous cellular sensors. Several recent studies reported modulation of different TRP channels by phosphoinositides, in particular by phosphatidylinositol 4,5-bisphosphate (PIP₂). In most cases, PIP₂ promotes TRP channel activation. Here we provide a brief overview of current insights and controversies about the mechanisms and structural determinants of PIP₂–TRP channel interactions, and zoom in on the regulation of the Ca²⁺- and voltage-gated TRPM4 by phosphoinositides.     

Modulation of IgE response by phytohemagglutinin

The effect of the administration of phytohemagglutinin (PHA) on the IgE response was studied. RF mice were immunized with OA in aluminum hydroxide gel and PHA was injected 1 or 2 days before the immunization in doses of 80 or 1 microliter. Results show that PHA injected on day -1 induces suppression and PHA administered on day -2 induces some stimulation in the IgE response. This effect is independent of the PHA doses used and does not affect the anti-OA hemagglutinin production.     

Modulation of chemokines by poxvirus infections

Viruses that successfully replicate within the host have devised strategies to subvert or evade the challenges posed by the innate and adaptive immune responses. Many investigators are now beginning to dissect the diverse and complex interactions involving chemokines, chemokine receptors and viral infection. In recent years, much attention has been focused on the role of chemokines in antiviral defense.     

Modulation of Antigen-Antibody Complexations by Immunoglobulins

In this investigation, the modulating effects of non-immune human IgG and rheumatoid factors (RFs) on antigen-antibody complexations were studied. Non-immune human IgG, as well as RF, were found to inhibit the binding of antigen to specific antibodies of both human and rabbit origin. In addition, human immunoglobulins were also able to modify the composition of preformed antigen-antibody complexes. The effects were detected by immunological methods in two different antigen-antibody systems (human serum albumin-rabbit anti-HSA and tetanus toxoid-human anti-TT). Changes in biological activities could be followed by employing enzymes (glucose-6-phosphate dehydrogenase and human placental alkaline phosphatase) as antigens. The outcome of the effects was found to be dependent on the ratio of antigen to antibody, the antigen-binding properties of the antibody and its origin, and on the properties of the immunoglobulins added. The observed changes could not be explained only by the presence of specific antibodies in the immunoglobulin preparations. The ability of immunoglobulins to modulate antigen-antibody complexations may provide a rationale for the large amounts of non-specific immunoglobulins in the circulation by preventing premature precipitation and promoting the elimination of antigenic molecules.     

Modulation of purinergic neurotransmission by ecto-ATPase

The role of ecto-ATPase in modulating the purinergic component of neurotransmission in the guinea-pig vas deferens has been investigated using ARL 67156, a recently developed inhibitor of ecto-ATPase. ARL 67156 rapidly and reversibly potentiated neurogenic contractions in a concentration-dependent manner. ARL 67156 also potentiated contractions evoked by exogenous ATP, but had no effect on those to the stable analogue α,β-methyleneATP or on those to noradrenaline and KCl in the presence of the P₂-purinoceptor antagonist PPADS. These results are consistent with an inhibitory action of ARL 67156 on ecto-ATPase and suggest that ecto-ATPase modulates purinergic neurotransmission in the guinea-pig vas deferens.     

Modulation of T-cell function by gliomas

Patients with primary intracranial tumors (gliomas) exhibit a profound decrease in immunity, the mechanism of which has, until recently, remained obscure. Here Thomas Roszman, Lucinda Elliott and William Brooks reveal that T cells obtained from these patients exhibit defects in interleukin 2 secretion and in expression of the high-affinity IL-2 receptor and they discuss the role played by immunosuppressive factors produced by gliomas in inducing these defects.     

Modulation and metamodulation of synapses by adenosine

The presence of adenosine in all nervous system cells (neurones and glia) together with its intensive release following insults makes adenosine as a sort of ‘regulator’ of synaptic communication, leading to the homeostatic coordination of brain function. Besides the direct actions of adenosine on the neurosecretory mechanisms, to tune neurotransmitter release, adenosine receptors interact with other receptors as well as with transporters as part of its attempt to fine-tune synaptic transmission. This review will focus on examples of the different ways adenosine can use to modulate or metamodulate synapses, in other words, to trigger or brake the action of some neurotransmitters and neuromodulators, to cross-talk with other G protein-coupled receptors, with ionotropic receptors and with receptor kinases as well as with transporters. Most of these interactions occur through A2A receptors, which in spite of their low density in some brain areas, such as the hippocampus, may function as amplifiers of the signalling of other mediators at synapses.