多巴胺激动剂阿朴吗啡对东莨菪碱诱导小鼠学习记忆障碍的影响

目的：研究多巴胺（DA）对小鼠学习记忆障碍的影响及其机制。方法：实验1采用腹腔注射东莨菪碱0．3mg／kg（SCOP 0．3,n=10）和3．0mg／kg（SCOP3．0）,连续注射60d,在第53天和60天用避暗法测定记忆行为,第60天处死动物后取脑用免疫组化的方法测定TH-ir和Fos-ir的表达。实验2根据实验1结果造小鼠记忆障碍的模型后将小鼠分成4组,1组腹腔注射生理盐水（NS）,其他3组腹腔注射阿朴吗啡0．1mg/kg（APO 0．1）、0．5mg／kg（APO 0．5）和2．0mg／kg（APO 2．0）,每组10只动物,连续30d。在注射阿朴吗啡第23天和30天测定避暗行为。第30天处死动物后取脑用免疫组化的方法测定Fos-ir和TH-ir的表达。结果：避暗法测定记忆发现东莨菪碱抑制小鼠的记忆。第60天,东莨菪碱3．0mg／kg组（SCOP3．0）的潜伏期比NS组显著缩短,仅是NS组的1／4（P〉0．05）,错误次数比Ns组增加了大约4倍（P〉0．05）,SCOP 0．3组的潜伏期和错误次数与NS组没有明显差异。免疫组化结果表明在伏隔核和海马区的CAl和CA3的Fos-ir细胞数明显降低（P〈0．01）,且被盖腹侧区的酪氨酸羟化酶（TH-ir）和共表达TH／Fos-ir细胞显著减少（P〈0．01）。注射阿朴吗啡后明显缓解了小鼠的记忆障碍,且腹侧被盖区TH-ir细胞增加（P〈0．05）。结论：阿朴吗啡明显减轻东莨菪碱诱导的小鼠记忆障碍,是通过增强腹侧被盖区多巴胺神经元的活性来实现的。     

乳酸菌肽聚糖部分免疫增强作用的研究

以小鼠为实验材料研究了肽聚糖部分免疫学活性,结果表明:小鼠腹腔注射肽聚糖后,相比对照组而言, Z8、Z17肽聚糖组巨噬细胞(MΦ)吞噬率、吞噬指数都明显提高,血清溶菌酶活性显著增强,统计学分析差异极显著(P＜0．01)。肽聚糖对鸡新城疫疫苗免疫增强效果的观察表明,与对照组相比,Z8、Z17肽聚糖组能明显提高新城疫抗体水平,并使抗体高峰水平维持时间延长。同时动物实验也表明,两个肽聚糖组间活性差异不显著,没有特异性。     

腹腔注射乙酰唑胺对大鼠氧惊厥潜伏期的影响

为探讨脑血流调节与氧惊厥的关系,本研究在复制大鼠氧惊厥模型的基础上,采用行为学方法测定氧惊厥潜伏期,并测定脑皮质氧化指标内二醛（maleic dialdehyde,MDA）含量,采用腹腔注射不同剂量脑血管扩张药物乙酰唑胺（acetazolamide,ACZ）,以及联合注射ACZ及其拈抗刺吲哚美辛（indomethacin,IND）后,观察脑血管扩张对氧化状态以及氧惊厥潜伏期的影响。结果观察到：（1）腹腔注射ACZ（不小于7．5mg／kg体重）后,氧惊厥潜伏期明显缩短（P〈0．05）,剂量越大,缩短越明显。腹腔注射IND对氧惊厥潜伏期无显著影响。腹腔注射IND（20mg／kg体重）,30min后再注射ACZ（7．5mg／kg体重）,ACZ的氧惊厥潜伏期缩短作川被对抗（P〈0．05）。（2）腹腔注射ACZ7．5mg／kg后,与各组相比,6及16min暴露后,脑组织MDA含量明显增多（P〈0．01,P〈0．05）;腹腔注射IND对脑皮质MDA含量无显著影响;在预注射IND,再注射ACZ后,MDA含量显著降低（P〈0．01,P〈0．05）。结果表明,ACZ外周注射加重氧化损伤,缩短氧惊厥潜伏期;而IND可以对抗其氧惊厥潜伏期缩短作用以及氧化损伤加重作用,碳酸酐酶活力变化很可能是通过影响脑血管状态而影响氧化损伤以及氧惊厥潜伏期。     

乳酸菌肽聚糖部分免疫增强作用的研究

以小鼠为实验材料研究了肽聚糖部分免疫学活性,结果表明:小鼠腹腔注射肽聚糖后,相比对照组而言, Z8、Z17肽聚糖组巨噬细胞(MΦ)吞噬率、吞噬指数都明显提高,血清溶菌酶活性显著增强,统计学分析差异极显著(P＜0．01)。肽聚糖对鸡新城疫疫苗免疫增强效果的观察表明,与对照组相比,Z8、Z17肽聚糖组能明显提高新城疫抗体水平,并使抗体高峰水平维持时间延长。同时动物实验也表明,两个肽聚糖组间活性差异不显著,没有特异性。     

褪黑素对吗啡戒断小鼠下丘脑弓状核和中脑导水管周围灰质中β-内啡肽含量的影响

本文在观察腹腔注射褪黑素（melatonin,MEL）拮抗吗啡依赖小鼠纳洛酮催促戒断反应的同时,采用放射免疫分析法、免疫组织化学法,结合计算机图像处理技术,测定其对小鼠中脑导水管周围灰质（periaqueductal grey,PAG）、下丘脑弓状核（hypothalamic arcuatenucleus,Arc）中β-内啡肽（p-endorphin,β-EP）含量的影响。结果表明,MEL（80mg／kg体重）显著抑制吗啡依赖小鼠戒断反应（P〈0．05）的同时,可显著增加其中脑PAG中β-EP含量（P〈0．05）,减弱Arc中β-EP样免疫阳性反应强度（P〈0．05）。上述结果提示,MEL可提高吗啡戒断小鼠中脑PAG中β—EP含量,降低Arc中β-EP含量。     

诱导子对藏红花悬浮培养细胞生产藏红花色素的影响

考察壳聚糖（chitosan）、壳寡糖（chitosanoligosaccharides,COS）、茉莉酸甲酯（methyljasmonate,MJ）、水杨酸（salicylicacid,SA）和Cu2＋等诱导子对藏红花悬浮培养细胞生长和藏红花色素合成的影响。结果表明：在实验考察浓度范围内,壳寡糖（1～500mg／L）和较低浓度壳聚糖（≤10mrdL）、MJ（≤10μmol／L）、SA（≤10μμmol／L）和Cu2＋（≤1μmoL／L）对细胞生长无显著影响;较高浓度壳聚糖（≥100mg／L）、MJ（≥100μmol／L）、SA（≥100μmoL／L）和cu“（≥10μmoL／L）显著抑制细胞生长。5种诱导子对藏红花色素合成的诱导效果不同,并且与诱导子作用浓度和添加时间有关。MJ诱导效果最好,在细胞培养第0天添加终浓度100仙moL／LMJ,藏红花色素含量（以1克干细胞计）达到28．57mg,比对照提高177．9％。其次是cu“,在细胞培养第4天添加终浓度500μmoL／LCu2＋,色素含量达到19．82mg,比对照提高108．2％。再次是壳聚糖和壳寡糖,在细胞培养第14天分别添加终质量浓度100mg／L壳聚糖和壳寡糖,色素含量分别达到18．33和17．39mg,比对照提高69．1％和69．0％。最后是SA,在细胞培养第14天添加终浓度10μmoL／LSA,色素含量达到14．65mg,比对照提高45．4％。     

梓醇对鱼藤酮损伤小鼠的记忆、抗氧化能力的影响及安全性评价

目的:研究梓醇对鱼藤酮损伤小鼠的学习记忆能力及皮层抗氧化系统的影响,并对其安全性进行评价.方法:腹腔注射鱼藤酮建立小鼠皮层抗氧化系统损伤模型,腹腔注射给药21 d后进行Y迷宫试验,再测定各组小鼠皮层谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽S-转移酶(GST)、丙二酫(MDA)、谷胱甘肽(GSH)水平;梓醇安全性评价采取小鼠急性毒性试验和大鼠长期毒性试验.结果:梓醇能够改善小鼠的迷宫成绩,增强GSH-PX活性和GSH含量,降低GST活性和MDA含量,抑制LDH的释放.小鼠腹腔注射给药梓醇的LD50为206.5mg/kg.;大鼠尾静脉注射90天,未见动物出现血液学、血液生化及主要脏器的毒性变化.结论:梓醇能改善鱼藤酮损伤小鼠的记忆能力,减轻皮层氧化应激损伤;长期使用无明显的毒副作用.     

从豆制品废水厌氧发酵液分离的一株新的产甲烷球菌

用Hungate厌氧技术,从豆制品废水厌氧发酵液中分离到一株细胞直径为0.5--1.2μm的球形产甲烷细菌,编号8508。该菌株利用H2／CO2和甲酸盐生长产甲烷。生长要求乙酸盐、酵母膏和酪素水解物。最佳生长要求0．5--1．0％的NaCl或MgCl20生长的最适温度为35℃,最适pH 7．0--7．3。DNA的G+C含量为41mol％。菌株8508可能是甲烷球菌属(Metha-nococcus)中的一个新种,但还要通过DNA杂交、荧光抗体等测定证实。     

灵芝孢子粉氨基酸、脂肪酸及元素组成的研究

从灵芝Ganoderma lucidum 孢子粉中检出18种常见氨基酸,总量为7．29～7．71mg／100mg 其中甲硫氨酸含量高达3.30～3.48mg／100mg,人体必需氨基酸含量占总量的694～70.4％。灵芝孢子粉含有棕榈酸(19.8％)、油酸(55.2％)、亚油酸(16.5％)以及少量的肉豆蔻酸、硬脂酸、廿碳烯酸及廿二碳四烯酸等。对56种元素进行定量或半定量分析,结果表明灵芝孢子粉碳氮比C/N=17.57：1,含有磷1.28％、硫0.87％、硅0.92％、钾1.64mg／g钠28μg／g、钙0.713mg/g、镁0.346mg／g、铁0.64mg／g、锌420μg／g、 铜127μg／g、锰11μg/g锶609μg／g等二十多种人体必需或有益的常量元素及微量元素。     

凝结芽胞杆菌对免疫功能影响的实验研究

目的 研究凝结芽胞杆菌（TQ33）对实验动物免疫功能模型的影响。方法 以鸡红细胞混悬液对小鼠腹腔注射,观察TQ33对小鼠腹腔巨噬细胞吞噬功能的影响;制备绵羊红细胞（SRBC）,观察血球凝集程度,测定血清溶血素;以靶细胞（YAC-1细胞）与脾细胞（效应细胞）的反应检测TQ33。对小鼠NK细胞活性的影响;采用淋巴细胞转化法观察TQ33对细胞免疫的影响;计算小鼠胸腺／体重及脾脏／体重为脏器系数观察TQ33对小鼠脏器的影响。结果 与对照组比较,TQ33显著增加小鼠腹腔巨噬细胞吞噬功能;对小鼠体液免疫功能有一定的增强作用;可增强小鼠NK细胞活性;对ConA诱导下的小鼠淋巴细胞转化有增强作用;对脏器系数没有显著的影响。结论 凝结芽胞杆菌具有明显的免疫调节作用,预示有良好的应用前景。     

环境污染物对巨噬细胞的影响及生物监测意义

随着工农业的发展,环境污染问题日趋严重。作为常见的环境污染物,二氧化硫经呼吸道转化为亚硫酸盐能引起多种呼吸系统疾病,并可能有促癌作用;重金属汞能引起中枢神经系统和多种器官损害,同时具有一定的免疫毒性,其危害已引起人们广泛关注。生物监测(bi0H10nitoring)是使用活     

In vivo and in vitro activation of alveolar macrophages by recombinant interferon-gamma

In vivo administration of recombinant interferon-gamma (rIFN-gamma) was previously shown to result in activation of the microbicidal activities of peritoneal macrophages (PM phi). Because macrophages at different anatomical sites vary in their functional capacities, we considered it of interest to determine whether administration of murine rIFN-gamma, either in vitro or in vivo, can enhance the microbicidal activity of resident alveolar macrophages (AM phi) and to compare the effects of rIFN-gamma on AM phi and PM phi. After incubation in vitro with rIFN-gamma, the antimicrobial activities of both murine AM phi and PM phi were enhanced, as assessed by their ability to inhibit replication of the intracellular parasite, Toxoplasma gondii. This effect was dose dependent for AM phi over a range of 0.1 to 1 U/ml and for PM phi over a range of 0.5 to 1000 U/ml. In this assay, the minimum dosage required for in vitro activation of AM phi was one-half that required for activation of PM phi, suggesting a greater sensitivity of AM phi to the in vitro activity of rIFN-gamma. Macrophages from both anatomical sites were also activated when rIFN-gamma was administered in vivo. This effect was dose dependent over a range of 10(3) to 10(5) U/mouse. Freshly harvested AM phi and PM phi from mice injected 24 hr earlier with 10(4) U rIFN-gamma by either the i.v. or i.p. routes markedly inhibited intracellular multiplication of Toxoplasma. In contrast, AM phi and PM phi from control mice permitted fourfold to ninefold increases in numbers of intracellular Toxoplasma. The anti-toxoplasma activity of AM phi and PM phi gradually diminished over a period of 3 days when assayed at successive 24 hr periods after a single i.v. injection of rIFN-gamma. At 3 days after injection, a substantial loss of anti-toxoplasma activity was observed with PM phi as compared with controls; residual anti-toxoplasma activity was still demonstrable in AM phi at 3 days. These results demonstrate that in vitro as well as in vivo treatment with rIFN-gamma confers on AM phi an enhanced antimicrobial activity. These findings provide a rationale for evaluating rIFN-gamma in the treatment of pulmonary infections, especially those due to opportunistic pathogens against which AM phi play a major role in host defense.     

Immune response in experimental animals immunized with Burkholderia pseudomallei surface antigens

The influence of the chromatographic fractions of B. pseudomallei surface antigenic complex (C, C1, D, H) on immune response in white rats and white mice was under study. These antigenic complexes were noted to produce perceptible stimulating effect on the immune system of white rats, in contrast to that of white mice. The immunization of the mice the above-mentioned fractions suppressed the phagocytic activity of peritoneal macrophages (PM) and slightly enhanced cell-mediated immunity. In experiments on white rats, fraction C induced the growth of specific antibody titers and stimulated the phagocytic activity of PM, as well as the indices of delayed hypersensitivity (DH). Fraction D showed a lower level of the induction of the phagocytic activity of PM and was inactive in the manifestation of cell-mediated immunity, but induced a high level of humoral immunity. Antigenic complexes C1 and H increased the phagocytic activity of PM and DH characteristics with a low level of antibody production. The studied fractions of the causative agent of melioidosis decreased the content of bactericidal cationic proteins (BCP) in rat blood neutrophils, and in mice a decreased content of BCP in phagocytes was registered. The fractions increased the activity of myeloperoxidase in blood neutrophils in mice and rats. As revealed with the use of immunoelectrophoresis, SDS PAAG electrophoresis and immunoblotting, the surface antigenic complex contained proteins of 18, 22, 39 kD and glycoproteins 42, 55, 90 kD. The latter glycoprotein was found in all the fractions under study, having protective properties.     

The effect of bone marrow depletion on prostaglandin E-producing suppressor macrophages in mouse spleen

The i.p. injection of Corynebacterium parvum (CP) into CBA/J mice effected increases in macrophage colony-forming cells (M-CFC) when spleen cells were cultured with L cell culture filtrate as a source of colony-stimulating factor. Significant increases in phagocytic macrophages (M phi) with Fc receptors for IgG2a and IgG2b immune complexes were additionally noted among the spleen cells in these mice. These M phi effectively inhibited Con A-induced lymphocyte proliferation, probably reflecting a 10-fold increase above normal controls in prostaglandin E to 47 ng/3 X 10(6) spleen cells/ml. To determine whether the suppressor M phi are immediate derivatives of splenic M-CFC, we tried to induce suppressor M phi by the injection of CP into mice depleted of bone marrow M-CFC by the earlier administration of the bone-seeking isotope, 89Sr. This procedure reduced M-CFC in the bone marrow to less than 1% of normal for more than 30 days. Monocytes in the blood fell to 5% of normal by day 10 and were 30% on day 30. Levels of resident peritoneal M phi showed relatively little change in this period. By contrast, splenic M-CFC increased to 20-fold higher than the "cold" 88Sr controls. CP-induced suppressor M phi activity, however, was sharply reduced in 89Sr marrow-depleted mice on day 10, despite the striking increase in M-CFC. There was a threefold increase in the number of phagocytic M phi binding IgG2a immune complexes, with no significant increase in IgG2b binding M phi. The kinetics of recovery of suppressor M phi activity showed that on days 20, 30, and 50 after 89Sr injection the activities reached 20%, 30%, and 70% of the "cold" control, respectively, and correlated with the recovery of significant levels of M-CFC in the bone marrow. Taken together, these observations suggest that splenic M-CFC are not an immediate source of PGE-suppressor M phi in vivo. It appears more likely that the CP-inducible suppressor M phi, in particular, originate from radiosensitive bone marrow cells or require for differentiation a microenvironment provided by bone marrow cells. The data also suggest that the expression of the Fc gamma 2b receptor and of suppressor activity by CP-induced splenic M phi are related phenomena.     

大豆提取物（CKBN）对免疫低下小鼠免疫功能的影响

目的观察大豆提取物（CKBN）对免疫低下小鼠免疫功能的影响。方法腹腔注射环磷酰胺（cyclophosphamide,CTX）建立免疫功能低下小鼠模型,观察1、25、50、100 mg/kg剂量CKBN对免疫低下小鼠免疫功能的影响。结果25 mg/kg组的CKBN可显著增加免疫低下小鼠的脾指数;25、50、100 mg/kg组均能明显抑制环磷酰胺对小鼠外周血白细胞数量的影响,1 mg/kg组可显著提高单核细胞百分率,50 mg/kg组可显著提高中性粒细胞百分率;100 mg/kg组的IgG2a水平高于环磷酰胺组;1、25、50 mg/kg可显著提高腹腔巨噬细胞的吞噬功能;25 mg/kg组可显著提高NK细胞杀伤活性。结论CKBN能显著增强CTX造成的免疫低下小鼠的免疫功能。     

细虫草胞外多糖对小鼠腹腔巨噬细胞免疫功能研究

本实验在体外条件下,以人工发酵培养的细虫草胞外多糖OgE、OgE-F1和OgE-F2作用于小鼠腹腔巨噬细胞RAW264.7,通过测定其对巨噬细胞的增殖率、代谢MTT活力、NO分泌和吞噬能力的影响,评价细虫草胞外多糖的免疫调节活性。结果表明,细虫草多糖对巨噬细胞无细胞毒性,且能促进巨噬细胞代谢MTT活力;在0.2mg/mL^1.0mg/mL浓度范围内,多糖呈剂量依赖性的促进巨噬细胞分泌NO水平和吞噬能力。本研究表明,细虫草多糖能有效地增强小鼠巨噬细胞的活性,潜在地可改善小鼠的先天性免疫调节。     

Calmodulin-dependent regulation of Ca,Mg-ATPase activity in plasma membranes of the swine myometrium

Highly purified plasma membrane (PM) preparations of pig myometrium were found to contain 0.91 +/- 0.22 microgram calmodulin per mg of PM protein. Treatment of membranes with 1 mM EGTA in the presence of 0.2 M NaCl causes the diminution of the calmodulin content down to 3% of the original level. The activity of Ca, Mg-ATPase is thereby decreased by 40%. Exogenous calmodulin restores the enzyme activity up to 1.94 +/- +/- 0.30 mumol Pi/mg protein/hour. The maximal activation of Ca, Mg-ATPase is observed with 10(-7) M calmodulin. Calmodulin increases the total ATPase activity of myometrium PM without affecting the Mg-ATPase activity. Trifluoroperazine (20 microM) diminishes the activating effect of exogenous calmodulin on Ca, Mg-ATPase. Calmodulin stimulates Ca, Mg-ATPase at low concentrations of Ca2+(10(-8)-10(-6) M) by decreasing Km for Ca2+ from 0.4.10(-6) M to 2.10(-8) M as well as by increasing Vmax--from 0,8 to 1.42 mumol Pl/mg protein/hour. It is supposed that the activating effect of calmodulin on Ca, Mg-ATPase is based on electrostatic interactions of Ca2+-free calmodulin with the enzyme.     

内蒙古地产紫沙参多糖免疫功能

给小鼠灌胃口服紫沙参多糖 ４００ ｍｇ· ｋｇ－１、８００ ｍｇ· ｋｇ－１,观察其连续给药对免疫功能的影响。结果显示：在５ｄ后能显著地增加小鼠耳肿胀度,提示紫沙参多糖能够增强二硝基氯苯诱导的小鼠迟发性变态反应（ＤＴＨ）;在７ ｄ后能显著地增加碳粒廓清指数Ｋ和吞噬指数α,增强单核巨噬细胞的吞噬功能,能显著地增加免疫器官胸腺、脾脏重量,增强机体免疫作用。试验采用国家中药二类新药云芝多糖 １０００ ｍｇ· ｋｇ－１作为阳性对照组。     

扇贝糖胺聚糖对感染HSV-Ⅰ小鼠免疫功能的影响研究

目的:研究扇贝裙边糖胺聚糖(glycosaminoglycan from Scallop Skirt,SS-GAG)对感染单纯疱疹病毒Ⅰ型(herpes simplex virus type,HSV-Ⅰ)小鼠免疫功能的影响。方法:通过在无菌条件下给予小鼠注射扇贝糖胺聚糖SS-GAG,连续11天,并在给药第三天给小鼠腹腔注射HSV-Ⅰ病毒悬液建立小鼠感染模型,用MTT等方法观察SS-GAG对HSV-Ⅰ感染小鼠腹腔巨噬细胞吞噬活性的影响、对脾脏指数、胸腺指数的影响以及对脾淋巴细胞转化能力等免疫指标的影响。结果:与病毒对照组相比,扇贝糖胺聚糖SS-GAG低剂量组、中剂量组、高剂量组均能显著增强HSV-Ⅰ感染小鼠的腹腔巨噬细胞的吞噬活性和HSV-Ⅰ感染小鼠的脾脏指数和胸腺指数(P0.01),并且能促进其脾淋巴细胞转化增殖能力(P0.01)。结论:扇贝糖胺聚糖在体内有一定的抗Ⅰ型单纯疱疹病毒作用。其抗病毒作用可能与增强机体免疫功能有关。     

Immune responsiveness and phagocytic activity of macrophages in streptozotocin (SZ)-induced diabetic mice

We succeeded in inducing different severities of diabetic state in C3H male mice by repeated intraperitoneal injections of various doses of SZ. SZ-induced diabetic mice were divided into four groups as follows: Group A, B, C and D. SZ, respectively, 3, 5 doses of 45 mg/kg, 5 doses of 60 mg/kg on consecutive days and one of a dose of 200 mg/kg BW. The degree of hyperglycemia and glycosuria were mild in group A and D. Group B was moderate and group C severe with ketonuria and loss of body weight. We investigated the immune response to anti-sheep red blood cells (SRBC) and the phagocytic activity of macrophages in the above mentioned various SZ-induced mice. Antibody forming activities (values of anti-SRBC plaque-forming cells (PFC) and serum agglutinin) were markedly depressed in all of SZ-diabetic groups. The degree of the suppression of antibody response to SRBC in SZ-diabetic mice corresponded with the severity of the diabetic state (C greater than B greater than A = D). However, the phagocytic activity of peritoneal macrophages in SZ-diabetic mice was as high as or higher than that in normal controls, using both latex beads and immune complex as test particles. Moreover, we observed that insulin treatment reversed the defect in the immune response in SZ-diabetic mice. These results indicate that the phagocytic activity of peritoneal macrophages was retained but the antibody response was impaired in the SZ-diabetic mice, and this suggested that the impaired antibody response may be a contributing cause of increased susceptibility to infections in a diabetic state.