番泻叶泻下与劳倦过度单,复因素脾虚模型的免疫学研究

目的 研究番泻叶泻下与劳倦过度单复因素脾虚模型在免疫学方面的改变。方法 通过免疫学８项指标的改变分析番泻叶泻下与劳倦过度单、复因素脾虚造模方法的优劣。结果 番泻叶泻下与劳倦过度单、复因素脾虚模型在特异玫瑰花结形成率、ＩｇＧ与ＩｇＭ含量、Ｔ细胞亚群比例、ＩＬ－２活性、ＮＫ活性、淋巴细胞转化率８项指标上存在着差异。结论 劳倦过度虽较番泻叶泻下所致脾虚程度为轻，但却不失为一种确切有效的，便于长期施加的脾     

大黄泻下与劳倦过度单、复因素造模脾虚小鼠过氧化与抗氧化改变的比较研究

目的：探讨单因素与复合因素造模法对脾虚动物模型生物膜结构和功能改变的规律及其机制。方法：70只小白鼠随机分为4组,即大黄泻下造模（A）组20只,劳倦过度造模（C）组20只,大黄泻上加劳倦过度造模（AC）组20只,空白对照（O）组10只。观察各组小白鼠丙二醛（MDA）、共轭双烯（CD）、过氧化氢酶（Cat)、超氧化物歧化酶（SOD）及过氧化物酶（GSH－Px）的变化,结果：3种方法塑造的脾虚小鼠模型均出现了体重下降,MDA、CD升高,Cat,SO,GSH-Px下降,且脂质过氧化损伤程度和抗氧化氧化酶活性下降程度以AC组为最重。结论：脾虚造模方法以大黄泻下加劳倦过度法为优,复因素脾虚造模法要优于单因素脾虚造模法。     

脾虚证动物模型的实验研究进展

从事脾虚证动物模型的实验研究已有20多年,从最早的大黄致慢性腹泻模型,到最近常用的病证结合模型,虽然思路不同,方法各异,但有一点应该肯定,各种模型在脾虚证实质研究的不同时期都起到了一定的推动作用。本文简要介绍各类脾虚证动物模型造模方法,以供同道们参考。1　根据中医理论复制动物模型1.1　泻下法制脾虚证动物模型用泻下法致脾虚是脾虚证模型最常用的造型方法,其中,绝大多数为苦寒泻下法。苦寒泻下法中最常用药物为大黄、芒硝、番泻叶、大承气汤、蓖麻油、玄明粉等。大黄脾虚模型是我国最早的脾虚模型之一,应用时间长,比较普及,并积…     

3种脾虚小鼠红细胞膜流动性变化的研究

目的：研究几种脾虚证模型小鼠红细胞（RBC）模流动性（LFU）的变化规律。方法：分别用大黄、番泻叶、利血平制作脾虚模型。用血细胞分析仪检测不同模型小鼠血常规指标的变化，用荧光偏振法检测不同模型小鼠RBC LFU和微粘度（η）的变化。结果：不同造模方法对小鼠血常规指标，除平均血细胞容积外并无明显影响，但均使3种模型小鼠RBV LFU降低，η增加，结论：RBC LFU有可能成为评价脾虚证的一个客观指标。     

类脾阴虚证大鼠病理模型的初步研究

探讨脾阴虚证大鼠颊理模型的造型方法，并对这种模型进行初步观察分析每天给ＳＤ大鼠胃饲番泻叶０．８ｇ，甲状腺８０ｍｇ，成类脾有虚证病理模型，观察造型前后阶段实验动物活动状况、大便性状等有关指标。结果：该模型既出现了稀烂便、食少、腹胀、体重下降等脾虚运化失司症状，又有饮水量增加，燥动不安等阴虚内热病机的外在表现。有别于脾阳虚对照组。结果提示：番泻叶、甲状腺片合用是建立脾阴虚证病理模型的有效方法之一。     

脾虚三证模型大鼠脂质过氧化损伤的比较

目的：探讨实验性脾虚大鼠脂质过氧化损伤的差异性,方法：采用饮食加劳倦等 合因素分别复制脾虚不同主型动物模型,观察各模型组和治疗组的脂质过氧化物（LPO）的含量和谷胱甘肽过氧化物酶（GSH－Px) ,超氧化物歧化酶（SOD）,心肌黄酶（DTD）活性变化。结果,各脾虚模型大鼠LPO呈不同程度升高,各种抗氧化酶活性不同程度下降,且且间差异显著,各治疗组药物具有降低LPO,升高抗氧化酶活性的作用,结论：脂质过氧化损伤是脾虚三证的共同症理生理基础。     

肺气虚证患者的免疫功能探析

目的：了解肺气虚证患者（哮喘、慢支）的免疫学表现。分组：共分四组进行观察,分别为肺气虚哮喘组、肺气虚慢支组、多脏器虚慢支组和健康对照组。观察指标：血清ＩｇＡ、ＩｇＧ、ＩｇＭ、唾液ＳＩｇＡ、淋巴细胞亚群ＣＤ４、ＣＤ８、ＣＤ４／ＣＤ８。结果：与健康组相比,三组患者均表现为免疫功能下降;肺气虚慢支组的免疫功能要好于多脏器虚组;肺气虚慢支组和肺气虚哮喘组的免疫功能未表现出明显差异。     

脾虚三证模型大鼠脂质过氧化损伤的比较

探讨实验性脾虚大鼠脂质过氧化损伤的差异性。方法采用饮食加劳倦等复合因素分别复制脾虚不同证型动物模型。观察各模型组和治疗组的脂质过氧化物(LPO)的含量和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物岐化酶(SOD)、心肌黄酶(DTD)的活性变化。结果各脾虚模型大鼠LPO呈不同程度升高,各种抗氧化酶活性不同程度下降,且组间差异显著。各治疗组药物具有降低LPO、升高抗氧化酶活性的作用。结论脂质过氧化损伤是脾虚三证的共同病理生理基础。     

3种方法建立小鼠脾虚模型过程中血清褪黑激素水平变化规律的研究

[目的]研究3种方法建立小鼠脾虚模型过程中血清褪黑激素(MT)水平的变化规律,进一步探讨MT在脾虚证中的作用.[方法]利用ELISA法检测血清MT水平,观察MT在建立利血平型、大黄型和偏食醋型小鼠脾虚模型过程中的变化规律.[结果]随造模时间的延长,3种脾虚模型动物血清MT水平变化过程明显不同,但文献中显示的3种脾虚模型建立成功天数,与笔者实验中MT水平低下所对应的天数恰好吻合.[结论]提示MT的改变较普遍地存在于脾虚的发病过程中,不仅可以作为某些脾虚证的特征参照指标,也可能是某些脾虚病症在某个阶段的的重要客观生化指标.     

慢性束缚应激联合番泻叶灌胃法制备IBS-D大鼠模型的量效及时效关系评价

目的观察不同番泻叶浓度、束缚时间及造模持续时间对腹泻型肠易激综合征(diarrhea predominant irritable bowel syndrome,IBS-D)大鼠模型造成的影响,筛选一种较为理想的IBS-D大鼠模型制作方法.方法 SD大鼠32只,雌雄各半.随机分为空白组、模型1组(0.2 g/mL番泻叶+束缚1 h)、模型2组(0.3 g/mL番泻叶+束缚1 h)、模型3组(0.2 g/mL番泻叶+束缚1.5 h),每组8只,雌雄各半.以造模7、10、14 d时腹壁撤退反射时的疼痛阈值评价其内脏敏感性,腹泻指数评价其腹泻程度,同时对肠黏膜的组织学改变进行评价.结果各组模型大鼠疼痛阈值在7、10、14 d均较空白组明显降低(P0.05);腹泻指数在7、10、14 d均较空白组明显增加(P0.05).模型2组的疼痛阈值较模型1组在7 d和14 d低(均为P=0.006),与模型3组比较差异不明显(P=1.000,P=0.198);模型2组的腹泻指数较模型1组和模型3组在3个时间点高(P0.05).组织学分析显示各组大鼠均无明显的炎症性表现.结论 3种造模方法在7、10、14 d均可建立IBS-D的动物模型,其中束缚1 h联合番泻叶0.3 g/mL灌胃的方法在内脏敏感性及腹泻指数上要优于其他两种造模方法.     

脾虚三证模型大鼠脂质过氧化损伤的比较

目的 :探讨实验性脾虚大鼠脂质过氧化损伤的差异性。方法 :采用饮食加劳倦等复合因素分别复制脾虚不同证型动物模型。观察各模型组和治疗组的脂质过氧化物 (L PO)的含量和谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物岐化酶 (SOD)、心肌黄酶 (DTD)的活性变化。结果 :各脾虚模型大鼠 L PO呈不同程度升高 ,各种抗氧化酶活性不同程度下降 ,且组间差异显著。各治疗组药物具有降低 L PO、升高抗氧化酶活性的作用。结论 :脂质过氧化损伤是脾虚三证的共同病理生理基础。     

Spleen and liver dendritic cells differ in their tolerogenic and cytokine induction potential

Dendritic cells (DCs) play an important role in induction of cellular immune responses. It seems that DCs that reside in different organs may be distinct in their ability to induce immune responses. This study was done to address the differences between spleen and liver DCs in induction of immune response and/or tolerance. CD11c+ DCs were separated from the liver and spleen of C57BL/6 mice and pulsed with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55. 6105 MOG35-55 pulsed spleen or liver DCs were injected in foot pad of different groups of mice. Control groups received unpulsed DCs. After 5 days, the mononuclear cells (MNCs) of the regional lymph nodes were isolated from immunized mice for cytokine assays and lymphocyte transformation test. To study the immunologic or tolerogenic effects of DCs, three weeks after immunization of mice with MOG pulsed liver or spleen DCs, experimental autoimmune encephalomyelitis (EAE) was induced in DC-immunized mice by injection of MOG along with complete Freund's adjuvant. Our results showed that spleen DCs were more potent in stimulating lymph node T cells as illustrated in lymphocyte transformation test. Moreover IL-10 production was higher in mice immunized with liver DCs compared with those immunized with splenic DCs (p=0.017). However, no significant difference in IFN-γ production was observed between two groups. We also found that liver DCs+MOG immunized mice displayed a significantly delayed disease onset compared with spleen DCs+MOG immunized mice and the control groups. The disease score was also milder in liver DCs immunized mice compared with other groups. It seems that the higher IL-10 production induced by the liver DCs may be one of the main factors in down regulation of immune responses in this organ. It can be concluded also that the liver DCs may inhibit the progress of EAE by shifting the cytokines profile.     

Influence of leptin in the development of hepatic fibrosis produced in mice by Schistosoma mansoni infection and by chronic carbon tetrachloride administration

BACKGROUND/AIMS: Leptin, a product of the obese (ob) gene is present in activated stellate cells. This study investigated whether leptin is essential for the development of hepatic fibrosis caused by various agents. METHODS: Control and ob/ob mice were infected with Schistosoma mansoni or were administered chronic carbon tetrachloride to cause hepatic fibrosis. RESULTS: Fibrosis developed in both ob/ob and control mice. However, the amount of histologically detectable fibrosis and the increase in liver hydroxyproline content was significantly greater in both models of fibrosis for treated controls than for treated ob/ob mice. Fibrosis was associated with higher secretion of TGFbeta1 from spleen cells of treated control than treated ob/ob mice. Chronic leptin administration in ob/ob mice infected with Schistosoma mansoni resulted in an increase in the amount of fibrosis caused by Schistosoma mansoni, eliminating any significant differences in the amount of fibrosis between infected ob/ob mice and control mice. It also eliminated any significant difference in TGFbeta1 secretion between the infected ob/ob and infected control mice. CONCLUSIONS: This study shows that leptin deficiency decreases but does not eliminate hepatic fibrosis produced by Schistosoma mansoni and carbon tetrachloride administration. The effect of leptin in potentiating fibrogenesis is most likely mediated by TGFbeta1.     

白细胞介素-12及白细胞介素-18致小鼠脾虚的研究

目的：观察白细胞介素-12(IL-12)及白细胞介素-18(IL-18)能否导致脾虚，研究脾虚与IL-12及IL-18的关系。方法：60只小鼠随机分为脾虚组、IL组和对照组。采用利血平制作脾虚动物模型组，IL组每日腹腔注射IL-12、IL-18。采用免疫分析技术检测3组小鼠血浆IL-12、IL-18的含量。结果：IL-12及IL-18引起明显脾虚证的表现，与利血平制作脾虚动物模型组相似。脾虚组和IL组血浆IL-12、IL-18的含量明显升高。结论：IL-12、IL-18可导致脾虚，血浆IL-12、IL-18的含量可作为脾虚证的实验室参考指标。     

Ultraviolet-A light prolongs survival and improves immune function in (New Zealand black x New Zealand white)F1 hybrid mice

Although ultraviolet (UV) light is generally harmful to patients with systemic lupus erythematosus, most clinical and immunologic studies of UV exposure have evaluated the effects of UV-B (280-320 nm). The long-wavelength UV-A band (320-400 nm), however, is less toxic than UV-B and has different immunologic actions. Therefore, we studied the effect of UV-A irradiation on survival and immunologic function in the (New Zealand black x New Zealand white)F1 hybrid mouse model of systemic lupus erythematosus. Twenty-one (New Zealand black x New Zealand white)F1 mice were treated with 3.5 joules/cm2/day of UV-A light for 5 days each week, beginning at age 10 weeks. A control group consisted of 20 untreated animals. All UV-A-irradiated mice survived to 32 weeks, compared with 12 of 20 mice in the nonirradiated group (P = 0.0013). Splenomegaly was significantly decreased in the irradiated mice (P less than 0.03). Mice that received UV-A treatment combined with depilation had significantly improved lymphocyte responses to phytohemagglutinin and lipopolysaccharide and significantly decreased levels of anti-DNA antibodies compared with mice that received neither treatment. Reductions in spleen size and anti-DNA antibody titer were significantly correlated with improved parameters of lymphocyte function. These results suggest that a relatively small dose of UV-A exerts significant therapeutic action in murine lupus, perhaps through an effect on immunologic regulation.     

Trypanosoma cruzi: deficient lymphocyte reactivity during experimental acute Chagas'' disease in the absence of suppressor T cells

Infection of mice with Trypanosoma cruzi has been shown to lead to an impaired ability of lymphocytes to proliferate in response to mitogenic stimulation which is manifested during the acute period of the disease. A possible involvement of suppressor T lymphocytes has been postulated by other authors and was investigated in this work as a part of our efforts to disclose the mechanisms underlying the immunologic deficiency. Spleen cells from acutely infected CBA/J mice readily exhibited unresponsiveness to stimulation with concanavalin A, phytohaemagglutinin or a bacterial lipopolysaccharide. However, these cells were unable to reduce the responses that normal syngeneic-mouse spleen cells mounted to these mitogens when cultured together in equal proportions. Furthermore, removal of the Lyt 2.1-bearing cells, known to include the suppressor T cell subpopulation, from infected mouse splenocyte suspensions, did not alter the deficient responsive status of the remaining cells. These results, together with the severe depletion of the T-cell compartment which occurs in the spleens of animals acutely infected with T. cruzi, do not support an important role of suppressor T lymphocytes in the noted deficiency in lymphoid cell reactivity to mitogens. Reduced numbers of responder cells, intrinsic lymphocyte alterations or suppression by cells other than T lymphocytes remain plausible explanations to be explored.     

Ethanol as a Possible Cofactor in the Development of Murine AIDS

Chronic ethanol (EtOH) abuse in humans leads to a variety of immuno-modulatory events that can alter resistance to a number of infectious agents. Whether alcohol abuse affects the susceptibility to human immunodeficiency virus infection or the subsequent development of acquired immune deficiency syndrome (AIDS) is a matter of extreme importance; however, available information in humans or animal models is limited. The goal of this study was to evaluate the effect of chronic EtOH feeding in mice on the development of immunodeficiency in the murine model of AIDS (MAIDS). C57BV6 mice were placed on the Lieber-DeCarli liquid EtOH diet pS% or 31% total caloric intake) or a nutrient-matched isocaloric Quid control diet. Seven days later, mice were infected with the LP-BMS murine leukemia virus mixture, and groups of infected and noninfected mice were assayed at defined time points postinfection for antigen-specific and nonspecific immune responses. In the absence of retroviral infection, chronic EtOH feeding (5–8 weeks) led to reductions in spleen weights, compared with isocaloric controls. In spite of reduced spleen size, mitogenic responses of spleen cells to concanavalin A (ConA) and lipopolysaccharide (LPS) were elevated in EtOH-fed mice, as compared with mice fed the control diet. Chronic EtOH feeding also enhanced the allogeneic mixed lymphocyte response and increased antigen-specific priming of both B-cells and CD4⁺ T-cells to the antigen, sheep red blood cells. In MAIDS-infected mice, chronic EtOH feeding delayed but did not prevent the onset of virus-induced immunodeficiency and MAIDS-induced autoantibody synthesis. In contrast to mice with MAIDS infection alone, infected mice fed an EtOH diet displayed significant mitogenic responses to ConA and LPS at 4 weeks postinfection; however, at 8 weeks postinfection, both groups were completely immunosuppressed. Liver damage was detected in all groups of EtOH-fed mice, as indicated by the elevated liver enzymes, ALT and‘ASR moreover, MAIDS infection did not alter the extent of liver damage caused by EtOH feeding. These data suggest that chronic feeding of the Lieber-DeCarli EtOH diet in mice can lead to immune enhancement and that under these conditions causes a delay in the onset of MAIDS. Whether these results are caused by the effects of chronic exposure of the immune system to EtOH or to elevated Went levels in the standard Lieber-DeCarli liquid EtOH diet is discussed.     

Ultraviolet-a light prolongs survival and improves immune function in (new zealand black × new zealand white)F1 hybrid mice

Although ultraviolet (UV) light is generally harmful to patients with systemic lupus erythematosus, most clinical and immunologic studies of UV exposure have evaluated the effects of UV-B (280–320 nm). The long-wavelength UV-A band (320–400 nm), however, is less toxic than UV-B and has different immunologic actions. Therefore, we studied the effect of UV-A irradiation on survival and immunologic function in the (New Zealand black x New Zealand white)F₁ hybrid mouse model of systemic lupus erythematosus. Twenty-one (New Zealand black x New Zealand white)F₁ mice were treated with 3.5 joules/cm²/day of UV-A light for 5 days each week, beginning at age 10 weeks. A control group consisted of 20 untreated animals. All UV-A-irradiated mice survived to 32 weeks, compared with 12 of 20 mice in the nonirradiated group (P = 0.0013). Splenomegaly was significantly decreased in the irradiated mice (P = < 0.03). Mice that received UV-A treatment combined with depilcation had significantly improved lymphocyte responses to phytohemagglutinin and lipopolysaccharide and significantly decreased levels of anti-DNA antibodies compared with mice that received neither treatment. Reductions in spleen size and anti-DNA antibody titer were significantly correlated with improved parameters of lymphocyte function. These results suggest that a relatively small dose of UV-A exerts significant therapeutic action in murine lupus, perhaps through an effect on immunologic regulation.