羊胎盘免疫调节因子对小鼠腹腔巨噬细胞免疫功能的影响

目的探讨羊胎盘免疫调节因子(GPIF)对小鼠腹腔巨噬细胞免疫功能的影响。方法采用巨噬细胞体外培养的方法。分3个实验组,对腹腔巨噬细胞分别给予0 .0 5 ,0 .1和0 .5mg/mlGPIF进行体外培养,培养结束后,测定腹腔巨噬细胞吞噬中性红的能力、对溴化四唑蓝(MTT)的还原能力,以及分泌一氧化氮(NO)和白细胞介素 1(IL-1)的量。结果与对照组比较,各浓度GPIF均有促进腹腔巨噬细胞吞噬中性红能力作用,且能显著提高腹腔巨噬细胞对MTT的还原能力,增加NO和IL-1的分泌量(P <0 .0 5 )。结论GPIF具有非特异性免疫增强作用     

何首乌对小鼠腹腔巨噬细胞功能的影响

为了解何首乌对小鼠腹腔巨噬细胞功能的影响,采用微量浊度法测定小鼠腹腔巨噬细胞介导的细胞毒活性;采用小鼠胸腺细胞检测法测定小鼠腹腔巨噬细胞白细胞介素-1的分泌活性;采用姬姆萨染色法检测小鼠腹腔巨噬细胞的吞噬功能。结果表明,各药物实验组小鼠腹腔巨噬细胞介导的细胞毒作用及泌白细胞介素-1的分泌活性明显增强(P<0.01);各药物实验组小鼠腹腔巨噬细胞的吞噬功能明显增强(P<0.01),提示何首乌能促进小鼠腹腔巨噬细胞功能。     

商陆皂甙甲抑制小鼠巨噬细胞和抗体生成

商陆皂甙甲(EsA)体外在0.01～10μmol·L^-1范围内,对小鼠腹腔巨噬细胞吞噬中性红和LPS诱导的巨噬细胞合成及释放白介素1都呈明显的抑制作用。体内给药2.5～5mg·kg^-1可显著减少绵羊红细胞致敏的小鼠血清溶血素的含量。提示EsA的抗炎作用可能主要通过抑制巨噬细胞的吞噬和分泌功能。EsA间接作用于B细胞,抑制抗体生成。     

甲磺酸加替沙星对小鼠非特异性免疫防御的调节作用

目的考察甲磺酸加替沙星(GFLX)对小鼠非特异性免疫防御的调节作用.方法采用小鼠腹腔巨噬细胞体内、体外及半体内吞噬杀死金葡球菌来反映药物对非特异性免疫系统的影响.结果0.5MIC GFLX体外有促进小鼠腹腔巨噬细胞的杀菌作用;0.5MIC GFLX预处理腹腔巨噬细胞后,能显著提高腹腔巨噬细胞的吞噬及杀菌能力;静脉注射(20mg*kg-1)后巨噬细胞体外也有促进吞噬及杀菌作用;预防性口服给药(2,20mg*kg-1)3d后,小鼠抗感染作用增强,存活率提高.结论GFLX有促进小鼠非特异性免疫防御的作用.     

小鼠腹腔巨噬细胞的分离培养与吞噬功能测定

目的:建立小鼠腹腔巨噬细胞体外分离培养的方法,并测定其体内吞噬功能.方法:0.5%淀粉生理盐水诱导小鼠腹腔产生巨噬细胞,体外分离培养并观察细胞形态;体内吞噬5%鸡红细胞悬液,测定细胞吞噬百分数和吞噬指数.结果:小鼠腹腔巨噬细胞活率＞95%,形态典型,形成良好细胞单层;平均吞噬百分率和吞噬指数分别为26%和0.28.结论:本方法可用于小鼠腹腔巨噬细胞培养研究.     

瓜蒌皮对环磷酰胺致免疫功能低下小鼠免疫功能的影响

目的:研究瓜蒌皮对环磷酰胺致免疫功能低下模型小鼠免疫功能的影响。方法:以ip环磷酰胺建立小鼠免疫低下模型,ig给予瓜蒌皮浓缩液后采用含药血清体外培养小鼠腹腔巨噬细胞,MTT法考察巨噬细胞的活性及其吞噬鸡红细胞的吞噬百分率和吞噬指数;测定小鼠体内巨噬细胞的吞噬指数和吞噬系数、血清溶血素含量、淋巴细胞的转化率。结果:瓜蒌皮能提高免疫抑制小鼠吞噬系数、血清溶血素含量,促进T淋巴细胞转化;能提高巨噬细胞的活性及其吞噬鸡红细胞的能力。结论:瓜蒌皮有提高免疫抑制小鼠免疫功能的作用。     

小叶黑柴胡多糖对小鼠腹腔巨噬细胞功能的影响

目的研究小叶黑柴胡多糖（BPs）对巨噬细胞免疫功能的影响。方法收集KM小鼠腹腔巨噬细胞,用不同质量浓度的BPs溶液(10、100、200 mg·L^-1)刺激,检测巨噬细胞吞噬E.codi、趋化和分泌一氧化氮（NO）的功能。结果 HPs各个浓度组均能显著促进巨噬细胞吞噬E.codi和趋化作用（P<0.001）,但对巨噬细胞分泌NO无明显影响;BPs 100、200 mg·L^-1可明显抑制脂多糖诱导的巨噬细胞分泌NO（P<0.05）。结论 BPs可增强巨噬细胞免疫功能,但能抑制脂多糖诱导的炎症介质分泌。     

微囊藻毒素-LR对小鼠巨噬细胞吞噬功能及活性氧水平的影响

目的观察微囊藻毒素LR(MC-LR)对原代和传代巨噬细胞功能的影响。方法取BALB/c小鼠腹腔巨噬细胞,体外培养液中分别加入终浓度为1,10,100和1000nmol.L-1的MC-LR,同时以巨噬细胞株RAW264.7为对照,分别采用中性红吞噬实验和二氢罗丹明123探针检测实验,测定细胞吞噬活性和细胞内活性氧(ROS)水平。结果MC-LR对小鼠腹腔巨噬细胞的吞噬功能有浓度依赖的抑制作用。当MC-LR浓度高于10nmol.L-1时,小鼠腹腔巨噬细胞的胞内ROS水平也明显降低。但MC-LR对小鼠巨噬细胞系RAW264.7细胞的吞噬功能和细胞内ROS水平均无明显影响。结论MC-LR可抑制小鼠腹腔巨噬细胞的吞噬功能和ROS水平,原代巨噬细胞对MC-LR的敏感性高于传代细胞RAW264.7。     

猫爪草提取物对正常小鼠免疫功能的影响

目的研究猫爪草提取物对正常小鼠腹腔巨噬细胞吞噬功能的影响。方法以生理盐水作为空白对照,以香菇多糖片作为免疫研究的阳性对照,对猫爪草的猫爪草多糖、石油醚提取部位、乙酸乙酯提取部位、乙醇提取部位的提取物首次进行药理学筛选。结果在猫爪草各类提取成分对正常小鼠腹腔巨噬细胞吞噬功能影响的研究中,以猫爪草多糖对正常小鼠腹腔巨噬细胞吞噬功能的提高作用为最好,猫爪草脂溶性成分如猫爪草石油醚提取物有提高正常小鼠腹腔巨噬细胞吞噬指数的趋势。结论猫爪草多糖对正常小鼠腹腔巨噬细胞吞噬功能作用最强。     

大豆多糖对S_（180）荷瘤小鼠免疫调节作用的研究

目的从免疫学角度探讨大豆多糖对荷瘤小鼠抗肿瘤作用的机制。方法采用分光光度计测定大豆多糖对S180荷瘤小鼠巨噬细胞一氧化氮生成量的影响,利用酶标仪测定大豆多糖对S180荷瘤小鼠腹腔巨噬细胞吞噬功能的影响,定量溶血分光光度法检测B细胞功能。结果与对照组比较,大豆多糖各组均能显著提高小鼠巨噬细胞的吞噬活性,同时能明显提高荷瘤小鼠巨噬细胞产生一氧化氮的能力,并能使体内B淋巴细胞数量增加而提高抗体生成量。结论大豆多糖通过调节荷瘤小鼠免疫功能发挥抗肿瘤作用。     

白头翁糖蛋白的分离纯化及其性质

从中药白头翁根的水提取液中分离纯化得均一的糖蛋白组分PcG－A。它由木糖和葡萄糖组成，摩尔比为1．5：1，分子量6．25×104，糖含量61．8％，并含有10种氨基酸。初步分析表明PcG－A为非O-连接的糖蛋白。     

黑灵芝多糖对体外培养的小鼠腹腔巨噬细胞功能的影响

目的研究黑灵芝多糖对小鼠腹腔巨噬细胞功能的影响。方法用不同浓度的黑灵芝多糖作用于正常的和LPS活化的腹腔巨噬细胞;测定巨噬细胞代谢MTT活力;Griess法测定NO的产生;ELISA法检测巨噬细胞培养上清中TNF-α、IL-1β的分泌水平。结果黑灵芝多糖对细胞代谢MTT活力有增强作用;在20～160mg·L-1范围内,多糖呈剂量依赖性地促进正常的巨噬细胞分泌NO、TNF-α、IL-1β,增强免疫;而巨噬细胞经LPS激活后,与LPS组比较,多糖不同程度地抑制NO、TNF-α、IL-1β的过量分泌。结论黑灵芝多糖能有效地增强小鼠腹腔巨噬细胞的免疫,可改善LPS对小鼠腹腔巨噬细胞的诱导作用。     

松果菊苷对衰老小鼠免疫功能和线粒体DNA相对含量的影响

目的观察肉苁蓉提取物松果菊苷(ECH)对实验性小鼠免疫功能和肝细胞线粒体DNA相对含量的影响。方法小鼠皮下注射10%D-半乳糖10ml.kg-1,每天1次,连续8wk,建立亚急性衰老模型。阳性组和松果菊苷各组同时灌胃给于维生素E40mg·kg-1和ECH20、40、60mg·kg-1,每天1次。采用酶联免疫吸附试验(ELISA)法测定血清中IL-2、IL-6含量;中性红实验测定小鼠腹腔巨噬细胞吞噬功能;MTT法检测ConA诱导的小鼠脾淋巴细胞增殖转化;SDS碱变性法测定肝细胞线粒体DNA相对含量。结果与正常组比较,模型组小鼠血清IL-2含量,小鼠腹腔巨噬细胞吞噬功能和淋巴细胞增殖反应均下降,IL-6和肝脏线粒体DNA相对含量升高。ECH各剂量组和维生素E阴性对照组均能提高衰老小鼠血清IL-2含量、小鼠腹腔巨噬细胞吞噬功能和淋巴细胞增殖反应,降低IL-6和肝细胞线粒体DNA相对含量。结论松果菊苷能够提高机体的免疫功能,降低衰老小鼠肝细胞线粒体DNA相对含量,可能是其延缓衰老的作用机制之一。     

灵芝多糖肽拮抗吗啡的免疫抑制作用的体外试验

目的··:研究灵芝多糖肽(GPP)对吗啡所致免疫抑制的拮抗效应。方法··:采用中性红法检测小鼠腹腔巨噬细胞吞噬功能;采用[3H]TdR参入法测定淋巴细胞增殖反应;分别采用胸腺细胞增殖法和依赖IL-2和HT-2细胞株测定IL-1和IL-2生成。结果··:体外GPP50-800μg·ml-1可以不同程度地翻转高浓度吗啡所致的巨噬细胞吞噬功能降低,IL-1/IL-2产生减少及淋巴细胞增殖功能减退,使之恢复正常。结论··:提示GPP直接地使遭受抑制的免疫细胞的功能得以恢复,产生功能性拮抗作用。     

Differential effects of acyclic nucleoside phosphonates on nitric oxide and cytokines in rat hepatocytes and macrophages

Acyclic nucleoside phosphonates (ANP) are virostatics effective against viruses like hepatitis B virus and human immunodeficiency virus. Our previous reports indicated immunomodulatory activities of ANP in mouse and human innate immune cells. Recently, evidence has increased that hepatocytes may play an active role in immune regulation of the liver homeostasis or injury. In this study we investigated possible immunomodulatory effects of ANP on rat hepatocytes and macrophages. Nitric oxide (NO) production and secretion of cytokines (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-13, IL-18, IFN-γ, TNF-α and GM-CSF) were analyzed under in vitro conditions. Test compounds included: 9-[2-(phosphonomethoxy)ethyl]adenine (PMEA; adefovir); 9-[2-(phosphonomethoxy)ethyl]-2,6-diaminopurine (PMEDAP); (R)- and (S)-enantiomers of 9-[2-(phosphonomethoxy)propyl]adenine [(R)-PMPA; tenofovir] and [(S)-PMPA]; 9-[2-(phosphonomethoxy)propyl]-2,6-diaminopurine [(R)-PMPDAP] and [(S)-PMPDAP]. The group of test compounds also included their N(6)-substituted derivatives. Some of ANP which are able to induce NO production and cytokine secretion in cultured macrophages possess the same immunobiological activity in isolated hepatocytes. The extent of responses is in range of LPS/IFN-γ stimulation in both types of cells. The effects of active ANP on NO expression and cytokine secretion are dose- and time-dependent. Interestingly, the spectrum of detected cytokines induced by ANP is broader in hepatocytes. The results also confirm immunomodulatory effects of some ANP on rodent macrophages. Moreover, we demonstrate for the first time immunobiological reactivity of primary rat hepatocytes induced by exogenous ANP compounds. The potential of hepatocytes to synthesize cytokines can contribute to better understanding of liver immune function and can serve for pharmacological intervention in liver diseases.     

A new target for the treatment of inflammatory bowel disease: Interleukin-37

Interleukin (IL)-37 belongs to the IL-1 cytokine family. It has anti-inflammatory effects on numerous autoimmune diseases such as asthma, psoriasis, inflammatory bowel disease (IBD), systemic lupus erythematosus (SLE), multiple sclerosis (MS) and rheumatoid arthritis (RA). Mechanistically, IL-37 plays an anti-inflammatory role by regulating the expression of inflammatory factors in two ways: binding extracellular receptors IL-18R or transferring into the nucleus with Smad3. IBD is a kind of idiopathic intestinal inflammatory disease with unknown etiology and pathogenesis. Recent researches had proved that IL-37 is negatively involved in the pathogenesis and development of IBD. Among various inflammatory diseases, IL-37 has been shown to regulate inflammatory development by acting on various immune cells such as neutrophils, macrophages (Mϕ), dendritic cells (DCs), T cells and intestinal epithelial cells. This review summarizes the biological role of IL-37, and its immunoregulatory effects on the immune cells, especially anti-inflammatory function in both human and experimental models of IBD.     

Curcumin inhibits Th1 cytokine profile in CD4+ T cells by suppressing interleukin-12 production in macrophages.

1 Interleukin-12 (IL-12) plays a central role in the immune system by driving the immune response towards T helper 1 (Th1) type responses which are characterized by high IFN-gamma and low IL-4 production. In this study we investigated the effects of curcumin, a natural product of plants obtained from Curcuma longa (turmeric), on IL-12 production by mouse splenic macrophages and the subsequent ability of these cells to regulate cytokine production by CD4+ T cells. 2 Pretreatment with curcumin significantly inhibited IL-12 production by macrophages stimulated with either lipopolysaccharide (LPS) or head-killed Listeria monocytogenes (HKL). 3 Curcumin-pretreated macrophages reduced their ability to induce IFN-gamma and increased the ability to induce IL-4 in Ag-primed CD4+ T cells. Addition of recombinant IL-12 to cultures of curcumin-pretreated macrophages and CD4+ T cells restored IFN-gamma production in CD4+ T cells. 4 The in vivo administration of curcumin resulted in the inhibition of IL-12 production by macrophages stimulated in vitro with either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN-gamma and increased IL-4 production) in CD4+ T cells. 5 These findings suggest that curcumin may inhibit Th1 cytokine profile in CD4+ T cells by suppressing IL-12 production in macrophages, and points to a possible therapeutic use of curcumin in the Th1-mediated immune diseases.     

Tramadol differentially regulates M1 and M2 macrophages from human umbilical cord blood

Tramadol is an analgesic drug and relieves pain through activating μ-opioid receptors and inhibiting serotonin and noradrenaline reuptake. Emerging evidence shows that it also stimulates immune cells, including NK cells, splenocytes, and lymphocytes, and elevates IL-2 production. However, it remains unknown whether and how tramadol directly affects macrophages. To answer these questions, we collected human umbilical cord blood, isolated macrophages, and examined their responses to tramadol. Although tramadol did not alter resting macrophages and the antigen-presenting function in lipopolysaccharide-activated macrophages, it regulated M1 and M2 macrophages, which are, respectively, transformed by IFN-γ and IL-4. Interestingly, tramadol inhibits production and secretion of cytokines in M1 macrophages, but facilitates the production of inflammation-responding molecules, synthesized in M2 macrophages. We also found that STAT6 cascade pathway in M2 macrophages was significantly enhanced by tramadol. Therefore, this study reveals that tramadol regulates inflammation by inhibiting M1 macrophages (killing process), but promoting the function of M2 macrophages (healing process).     

黄芩有效成分SBM对炎症模型及免疫功能的影响

目的研究通过常温超高压方法得到的黄芩有效成分SBM的抗炎作用,并初步探讨其作用机制。方法观察SBM体外对淋巴细胞增殖、IL-1β合成的影响;观察给药后对佐剂性关节炎大鼠原发性及继发性病变、免疫功能及对甲醛诱导足肿胀、醋酸诱导腹腔渗出的影响。结果SBM(31.25～500mg.L-1)体外可明显抑制ConA诱导的小鼠脾淋巴细胞增殖及LPS诱导的腹腔巨噬细胞合成IL-1β;SBM(20mg.kg-1)灌胃给药可明显抑制佐剂性关节炎大鼠原发性及继发性足肿胀,并可抑制脾淋巴细胞增殖、IL-1β合成;SBM(20mg.kg-1)灌胃给药还可明显抑制甲醛诱导的大鼠足肿胀及醋酸诱导的腹腔渗出。结论SBM可通过抑制免疫细胞的功能及促炎因子的产生发挥抗炎作用。     

山香圆总黄酮体外对大鼠佐剂性关节炎免疫功能的影响

目的观察山香圆总黄酮(totalflavonoidsofturpiniaargutaseen,TFS)体外对佐剂性关节炎(adjuvantarthritis,AA)大鼠免疫功能的影响。方法选择健康♂SD大鼠,采用弗氏完全佐剂(freundscompleteadjuvant,FCA)诱导AA大鼠模型:将同一批号的的卡介苗80℃水浴1h灭活,用灭菌液体石蜡配成10g·L-1的乳剂。d28处死大鼠,取AA大鼠的免疫细胞(脾细胞和腹腔巨噬细胞)体外给药培养并检测一些免疫指标:细胞增殖法检测ConA、LPS诱导的大鼠脾淋巴细胞增殖反应及IL-1、IL-2的分泌水平;放免法检测PGE2水平。结果与正常组相比,AA大鼠ConA、LPS诱导的脾淋巴细胞增殖功能低下,脾淋巴细胞产生的IL-2活性下降,LPS诱导的大鼠腹腔巨噬细胞产生的IL-1、PGE2水平明显升高。TFS(10-8~10-4)mg·L-1可纠正AA大鼠低下的脾淋巴细胞增殖反应和脾细胞IL-2的产生,降低AA大鼠腹腔巨噬细胞产生过高的IL-1和PGE2。结论山香圆总黄酮对AA大鼠的异常免疫功能具有调节作用。