SOD猕猴桃果汁对体液免疫、血清与红细胞丙二醛水平的影响

目的 研究超氧化物歧化酶（ＳＯＤ）猕猴桃果汁姑降低血清、红细胞丙二醛（ＭＤＡ）含量及提高机体免疫球白水平的作用。方法 测定ＳＯＤ弥猴桃果汁服用前后正常妇女红细胞ＭＤＡ及血清ＭＤＡ、免疫球蛋白ＩｇＧ、ＩｇＡ、ＩｇＭ的含量。结果 ＳＯＤ弥桃果汁服用后,红细胞与血清ＭＤＡ含量显著降低血清,免疫球蛋白ＩｇＧ、ＩｇＡ、ＩｇＭ的含量。结果 ＳＯＤ猕猴桃果取用后,红细胞与血清ＭＤＡ量显著降低,免疫球蛋白ＩｇＧ、     

白癜风动物模型的制备

连续应用５％氢醌２０,３０,４０天,使豚鼠皮肤黑色素明显减少,血清中ＭＡＯ和ＣｈＥ活性增加;免疫球蛋白ＩｇＧ,ＩｇＡ和ＩｇＭ增加,尤其是ＩｇＭ在用药４０天后的增加,与正常对照组比,有显著性差异,提示用５％氢酯使动物模拟白癜风作用。     

肿瘤坏死因子-α(TNF-α)对离体兔黄体细胞孕酮分泌的影响及其作用机制

肿瘤坏死因子α(ＴＮＦα)是免疫内分泌网络中引入瞩目的一种细胞因子。近几年来发现ＴＮＦα存在于大鼠、牛、兔和人卵巢中。ＴＮＦα抑制大鼠和人黄体细胞ｃＡＭＰ生成和孕酮分泌。但ＴＮＦα对兔黄体细胞机能活动的影响目前尚未见报道。本实验研究了ＴＮＦα对兔黄体细胞机能活动的作用,并探索其作用机制,旨在了解ＴＮＦα在黄体萎缩中的作用。1　材料和方法(1)药品　重组肿瘤坏死因子α,人绒毛膜促性腺激素(ｈＣＧ)、人促性腺激素(ＦＳＨ)、Ｍ199培养基于粉、孕马血清促性腺激素(ＰＭＳＧ)、孕酮放射免疫测定药盒、ｃＡＭＰ放射免疫测定…     

大鼠加速型抗肾小球基底膜（GBM）肾炎的研制

将正常兔ＩｇＧ与完全弗氏佐剂颈免疫大鼠,８天后注射亚致肾炎剂量的兔抗大鼠肾小球基底膜（ＧＢＭ）血清,结果大鼠尿蛋白量在注射该血清后第１天即明显升高,第３天达高峰;在第２１天时,血清肌酐显著升高。肾脏组织学检查：免疫荧光见第１天即有大鼠ＩｇＧ、Ｃ３和兔ＩｇＧ沿ＧＢＭ呈典型线状沉积;光镜见第１天肾小球内细胞数目明显增加,内皮细胞肿胀,肾小球内见中性粒细胞浸润,第７、１４．２１天时肾小球毛细血管丛系膜区增宽,系膜细胞增生,间质可见炎症细胞浸润,ＰＡＳＭ染色可见ＧＢＭ增厚,电镜见ＧＢＭ内有电子致密物线状沉积,上皮足突融合内皮窗孔消失,微血栓形成阻塞管腔,间质有细胞浸润和纤维化。     

细胞因子对脐血B细胞免疫球蛋白类别转换的调节

为了解细胞因子对新生儿Ｂ细胞免疫球蛋白类别转换的调节作用,在体外细胞培养的基础上,采用反向酶联免疫斑点法观察了脐血单个核细胞及添加重组细胞因子后脐血Ｂ细胞免疫球蛋白释放细胞数量（ＩｇＳＣｓ）。结果：正常脐血单个核细胞仅产生少量的ＩｇＳＣｓ。用抗ＣＤ３单抗刺激丝裂霉素Ｃ处理后的脐血Ｔ细胞,并补充ｒＩＬ－２、ｒＩＬ－４、ｒＩＬ－１０及其组合,可诱导脐血Ｂ细胞释放ＩｇＡ、ＩｇＧ和ＩｇＭ。这些结果提示：细胞因子的补充可促进体外新生儿Ｂ细胞免疫球蛋白的类别转换     

地塞米松、噻庚啶和山莨菪碱对LPS诱导大鼠肝脏TNFα表达的影响

地塞米松（Ｄｅｘ）、噻庚啶（Ｃｙｐ） 和山莨菪碱（Ａｎｉ） 对脂多糖（ＬＰＳ） 诱导的大鼠肝脏ＴＮＦα表达的影响。Ｗｉｓｔａｒ大鼠４０ 只, 静脉注射ＬＰＳ（ＥｃｏｌｉＯ１１１Ｂ４ ５ｍ ｇ／ｋｇ） 后, 立即静脉给予Ｄｅｘ ５ｍ ｇ／ｋｇ、Ｃｙｐ５ｍ ｇ／ｋｇ 或Ａｍ ｉ１０ｍ ｇ／ｋｇ,于ＬＰＳ攻击后２ｈ 取动物的肝脏,ＡＰＡＡＰ法进行ＴＮＦα免疫组织化学研究,Ｎｏｒｔｈ－ｅｒｎ 杂交分析ＴＮＦαｍ ＲＮＡ 表达水平。结果发现ＬＰＳ攻击后２ｈ, 肝脏ＴＮＦαｍ ＲＮＡ 表达水平显著增高, 肝脏枯否氏细胞胞浆内有大量的ＴＮＦα红染颗粒。Ｄｅｘ、Ｃｙｐ 或Ａｎｉ均能显著降低大鼠肝脏ＴＮＦαｍ ＲＮＡ 水平和ＴＮＦα含量。结果表明Ｄｅｘ、Ｃｙｐ 和Ａｎｉ均显著抑制ＬＰＳ诱导的ＴＮＦα基因表达, 可能有抗感染性休克作用。     

颌下腺表皮生长因子促进大鼠胃粘膜损伤的愈合

用免疫组织化学方法观察到雄性大鼠颌下腺有非常丰富的表皮生长因子样免疫活性物质,并且主要位于导管细胞中,颌下腺摘除使血清尤其是胃液ＥＧＦ水平显著降低,直至手术后第２８天仍然维持在较低水平。利用颌下腺摘除术清内源性ＥＧＦ后,冰乙酸涂抹造成的慢性胃溃疡愈合速度较假手术大鼠明显减慢,而补充相应剂量的外源性ＥＧＦ可使颌下腺摘除大鼠的溃疡愈合速度恢复到与假手术组引当水平。上述结果显示,颌下腺及其分泌的ＥＧＦ对     

抗人IgM单克隆抗体的研究—脾内免疫建立抗人IgM单克隆抗体杂交瘤细胞株

用多发性骨髓瘤病人血清中提纯的ＩｇＭ抗原,用脾内免疫ＢＡＬＢ／ｃ小鼠后与Ｓｐ２／Ｏ骨髓瘤细胞融合,获得了７株分泌人ＩｇＭ单克隆抗体的杂交瘤细胞株,分别命名为２５Ｇ１、２５Ｇ３、２５Ｇ４、２５Ｇ５、２５Ｄ２、２５Ｄ３和２５Ｄ５。注射同系小鼠后可诱生含较高效价抗人ＩｇＭ腹水（ＰＨＡ＝１２１２）。该杂交瘤细胞经组织培养传代半年,冻存１４个月后复苏,其分泌ＩｇＭ性能稳定。用ＰＨＡ、ＥＬＩＳＡ做人ＩｇＭ、ＩｇＧ、ＩｇＡ阻断试验,仅ＩｇＭ可阻断。用琼脂糖双扩散证明其与羊抗人ＩｇＭ有共同沉淀线     

应用单克隆抗体测定人弓形虫IgM抗体的研究

为了检测人血清弓形虫ＩｇＭ抗体,采用抗人ＩｇＭ单克隆抗体和特异性抗弓形虫单克隆抗体建立捕获ＥＬＩＳＡ法,并与ＰＣＲ方法进行了比较。结果检测１０６５份献血员血清,检出阳性３例,用ＰＣＲ方法检测呈阳性结果;检测２３例类风湿病人血清及２份弓形虫ＩｇＧ抗体阳性血清均为阴性反应。说明该方法不受类风湿因子（ＲＦ）和特异性ＩｇＧ抗体的干扰,同时也表明捕获ＥＬＩＳＡ检测人血清中弓形虫ＩｇＭ抗体特异性,敏感性良好。     

血清抗脂阿拉伯甘露糖抗体对活动性肺结核的诊断价值

目的 评价抗ＬＡＭ－ＩｇＧ检测对活动性肺结核的诊断价值。方法 采用ＬＡＭ为抗原,ＤＩＧＦＡ法检测２７５例活动性肺结核,１４５例非活动性肺结核病人,１３５例非结核病人和１５０例健康人血清中的ＬＡＭ－ＩｇＧ。结果 活动性结核病组抗ＬＡＭ－ＩｇＧ阳性率８５．１％,其中菌阳为９３．８％,菌阴组８０．３％,非活动性结核组１２例阳性,非结核组１０例阳性,健康组１１例阳性：血清抗ＬＡＭ抗体诊断结核病的敏感性为８５．１％,特异性９２．３％,准确性９０％,阳性预测值８７．６％,阴性预测值９０．６％。结论 提示血清抗ＬＡＭ－ＩｇＧ测定可用于诊断活动性结核病。     

Increased phagocytosis of outer segments in the presence of serum by cultured normal, but not dystrophic, rat retinal pigment epithelium

Cultured normal rat retinal pigment epithelium (PE) ingested six times more rod outer segments in the presence of 20% fetal bovine serum than in serum-free medium. PE cultured from Royal College of Surgeons (RCS) rats with hereditary retinal dystrophy, known to have a defect in vivo in the phagocytosis of shed outer segment tips, ingested amounts of outer segments comparable to normal PE in serum-free medium but did not show an increase in the presence of serum. In both strains of rat PE phagocytosis of latex spheres was similar in the absence of serum and was six-fold higher in the presence of serum, showing that the RCS phagocytic deficiency for outer segments in vitro is not due to a general defect in the phagocytic capacity of the cell. Increased phagocytosis of outer segments by normal PE was observed in the presence of the high molecular weight fraction of ultrafiltered serum but was not seen with serum that was heated at 93 degrees C or precipitated with 5% trichloroacetic acid. Bovine serum albumin had no effect on phagocytosis. These results are consistent with the idea that the phagocytosis of outer segments by cultured normal rat PE, but not by cultured RCS rat PE, is increased in the presence of a specific protein or other macromolecular component of fetal bovine serum.     

Phagocytic receptors on macrophages distinguish between different Sporothrix schenckii morphotypes

Sporothrix schenckii is a human pathogen that causes sporotrichosis, a cutaneous subacute or chronic mycosis. Little is known about the innate immune response and the receptors involved in host recognition and phagocytosis of S. schenckii. Here, we demonstrate that optimal phagocytosis of conidia and yeast is dependent on preimmune human serum opsonisation. THP-1 macrophages efficiently ingested opsonised conidia. Competition with d-mannose, methyl α-d-mannopyranoside, d-fucose, and N-acetyl glucosamine blocked this process, suggesting the involvement of the mannose receptor in binding and phagocytosis of opsonised conidia. Release of TNF-α was not stimulated by opsonised or non-opsonised conidia, although reactive oxygen species (ROS) were produced, resulting in the killing of conidia by THP-1 macrophages. Heat inactivation of the serum did not affect conidia internalization, which was markedly decreased for yeast cells, suggesting the role of complement components in yeast uptake. Conversely, release of TNF-α and production of ROS were induced by opsonised and non-opsonised yeast. These data demonstrate that THP-1 macrophages respond to opsonised conidia and yeast through different phagocytic receptors, inducing a differential cellular response. Conidia induces a poor pro-inflammatory response and lower rate of ROS-induced cell death, thereby enhancing the pathogen's survival.     

Secretion of glucagon and insulin in hypophysectomized rats: effect of tolbutamide.

Normal and hypophysectomized (hypox) rats, fed ad libitum, received intraperitoneal injections of tolbutamide (75 mg/kg/day) or of saline for 6 weeks. 24 h after the last injection, blood samples were taken for glucose, insulin and glucagon determinations. In normal rats, tolbutamide treatment did not alter serum glucose, insulin and glucagon, although it suppressed the secretion of insulin and glucagon by the pancreatic islets. In hypox rats, tolbutamide decreased serum glucose and insulin, elevated serum glucagon and stimulated the secretion of glucagon, but not that of insulin by the pancreatic islets. In addition, tolbutamide treatment increased the glucagon response to arginine in normal, but not in hypox rats. The serum glucose response to arginine was decreased by tolbutamide treatment and by hypophysectomy and, thus, appeared independent of the glucagon rise or preexisting glucagon level. We conclude that tolbutamide treatment decreased the secretion of glucagon and insulin in normal rats and stimulated that of glucagon in hypox rats, perhaps because of the low levels of insulin in the serum and in the pancreas of the latter. Our results are compatible with the hypothesis that the pancreatic action of tolbutamide is influenced by the pituitary.     

Effect of orexin-A on phagocytic activity of peritoneal macrophage in starved rats

The aim of this study was to investigate the effect of fasting-induced orexin-A (OXA) on inflammation and macrophage phagocytic activity. Fifty six male wistar rats were fasted for 36 h to stimulate OXA synthesis. In 24 rats, air pouches were induced subcutaneously in the intrascapular area. After (6 h) carrageenan injection into the pouches, the contents of the air pouches were removed. The exudate volume, protein content and cell count were measured. After the determination of fasting on inflammation, the peritoneal macrophages were collected from 32 rats to investigate the effect of fasting-induced OXA on macrophage phagocytic activity. Plasma OXA levels were markedly higher in fasted rats compared with control rats. The phagocytic capability of peritoneal macrophages was obtained as a percentage of phagocytosing macrophages and number of phagocytosed particles per cell. In spite of increased blood OXA level SB-334867, selective orexin type 1 receptor antagonist (10 mg/kg) did not change phagocytic activity of peritoneal macrophages. These findings indicate that 36 h fasting-induced OXA has no significant effect to phagocytosis of peritoneal macrophages.     

Relations between the changes of the phagocytic activity of the reticuloendothelial system and the alterations in protein and nucleic acids contents of the rat liver (author's transl)]

The phagocytic activity of the reticuloendothelial system (RES) was evaluated after a single oral administration of soya-bean oil to male rats (15 g/kg). 1. An emulsion of soya-bean oil administered to the rat by gastric intubation activated the phagocytosis of colloidal carbon; the stimulation appeared on the 2nd day after treatment and persisted up to the 3rd day. There was also a relation between the stimulation of RES activity, under our experimental conditions, and the increased level observed in the protein and nucleic acid contents of the liver. 2. In contrast, without emulsion, soya-bean oil depressed the phagocytic activity on the 2nd and 3rd days after administration of the oil. These changes were associated with a diminution in ribonucleic acid and protein contents of the liver. Although the mechanisms of soya-bean oil-induced alterations of phagocytic activity were not clarified, there was a relationship between the RES stimulation or inhibition and the modifications in nucleic acid and protein contents of rat liver.     

Effect of gonadotropin-releasing hormone on phagocytic leucocytes of rainbow trout

To clarify the role of gonadotropin-releasing hormone (GnRH) in the fish immune system, in vitro effect of GnRH was examined in phagocytic leucocytes of rainbow trout (Oncorhynchus mykiss). Gene expression of GnRH-receptor was detected by RT-PCR in leucocytes from head kidney. Administration of sGnRH increased proliferation and mRNA levels of a proinflammatory cytokine, tumor necrosis factor (TNF)-α, in trout leucocytes. Superoxide production in zymosan-stimulated phagocytic leucocytes was also increased by sGnRH in a dose-related manner from 0.01 to 100 nM. There was no significant effect of sGnRH on mRNA levels of growth hormone (GH) expressed in trout phagocytic leucocytes. Immunoneutralization of GH by addition of anti-salmon GH serum into the medium could not block the stimulatory effect of sGnRH on superoxide production. These results indicate that GnRH stimulates phagocytosis in fish leucocytes through a GnRH-receptor-dependent pathway, and that the effect of GnRH is not mediated through paracrine GH in leucocytes.     

Effect of hydrocortisone on peripheral blood phagocytic cells under beta-adrenoreceptors blockade

The effect of hydrocortisone (50 mg/kg body wt i.p.) under beta-adrenergic receptors blockade (four subcutaneous injections of propranolol in single dose of 5 mg/kg body wt with 3 h interval) on phagocytic activity and oxygen dependent microbicidal activity in NBT-test of peripheral blood phagocytic cells in male Wistar rats was investigated. It was established that hydrocortisone stimulated neutrophil phagocytic activity through 6, 24 and 48 h after hormone injection and decreased oxygen-dependent microbicidal activity of phagocytic cells in NBT-test. Hydrocortisone in vitro (500 ng/ml) decreased neutrophil phagocytic activity that indicated on realization of stimulating effect of hydrocortisone in vivo through complex of other indirect mechanisms. Administration of hydrocortisone led to depression of eosinophil phagocytosis and lesser decrease in monocyte phagocytic activity. Hydrocortisone effects were significantly modified under blockade of beta-adrenoceptors that indicated on its mediation by endogenous catecholamines through modulation of beta-adrenoceptor expression.     

Fate of intravenously administered particulate and lipoprotein cholesterol in the rat

Unesterified radioactive cholesterol, both bound to serum lipoproteins and dispersed in ethanol-saline, was injected into bile fistula and intact rats. Due to phagocytosis, mainly by the liver macrophages, intravenously injected cholesterol in ethanol-saline disappears from the bloodstream significantly faster than lipoprotein-bound cholesterol. Soon after the initial phagocytosis, the particulate isotopic cholesterol started to reappear in blood, reaching a maximal radioactivity in blood 10-24 hr after injection. Although the radioactive cholesterol reappears in serum in both esterified and unesterified form, it is likely that cholesterol is released from the phagocytic cells as unesterified cholesterol which is then esterified intravascularly or at other sites. In the bile fistula rats, somewhat more of the lipoprotein cholesterol than of the particulate cholesterol appeared in bile early after injection. However, cholesterol turnover calculated from a twopool model was the same for rats injected with lipoproteinbound or particulate cholesterol.     

NTPDase1 activity attenuates microglial phagocytosis

Purinergic signaling plays a major role in the regulation of phagocytosis in microglia. Interplay between P2 and P1 receptor activation is controlled by a cascade of extracellular enzymes which dephosphorylate purines resulting in the formation of adenosine. The ATP- and ADP-degrading capacity of cultured microglia depends on the expression of ecto-nucleoside triphosphate diphosphohydrolase 1 (CD39) and is several times higher when compared to astrocytes which lack this enzyme. In brain slices, deletion of CD39 resulted in a 50 % decrease of ADP-degrading ability, while the degradation of ATP was decreased to about 75 % of the values measured in wild-type brain tissue. Microglia in acute slices from cd39^?/? animals had increased constitutive phagocytic activity which could not be further enhanced by ATP in contrast to control animals. Pharmacological blockage of P2 receptors decreased the constitutive phagocytic activity to a similar base level in wild-type and cd39^?/? microglia. Activation of P1 receptors by non-hydrolysable adenosine analog significantly decreased phagocytic activity. Deletion of CD73, an enzyme expressed by microglia which converts AMP to adenosine did not affect phagocytic activity. Taken together, these data show that CD39 plays a prominent role in controlling ATP levels and thereby microglial phagocytosis.