精氨酸对创伤大鼠免疫调节作用的研究

研究了腹部创伤大鼠免疫功能的变化及精氨酸对创伤大鼠的免疫调节作用。结果显示：腹部创伤大鼠脾脏自发性抑制性Ｔ淋巴细胞活性明显增强，脾脏淋巴细胞白细胞介素２生成能力明显下降；应用精氨酸治疗能够明显地降低自发性抑制性Ｔ淋巴细胞活性，促进脾脏淋巴细胞白细胞介素２的产生。结果表明，创伤大鼠免疫功能明显下降，应用精氨酸治疗能够明显改善创伤大鼠的免疫功能，有助提高其抗感染力。     

消炎痛对阻塞性黄疸大鼠淋巴细胞IL－2及Ts活性的影响

阻塞性黄疸患者围手术期易感性明显高于非黄疸者，发病原因尚不完全清楚。本文研究了阻塞性黄疸大鼠脾脏淋巴细胞白细胞介素２（ＩＬ－２）生成能力及抑制性Ｔ淋巴细胞（Ｔｓ）功能的变化以及消炎痛的作用。结果表明。胆管结扎大鼠脾脏淋巴细胞ＩＬ－２生成明显下降，Ｔｓ细胞活性明显增强；消炎痛治疗使阻塞性黄疸大鼠脾脏淋巴细胞ＩＬ－２生成能力增强和ＴＳ细胞活性下降。提示阻塞性黄疸宿主免疫功能异常，可能是其围手术期易感性增高的原因之一，消炎痛有可能成为改善阻塞性黄疽病人免疫功能，降低感染易感性的有价值药物之一。     

消炎痛对阻塞性黄疸大鼠淋巴细胞IL－2及Ts活性的影响

阻塞性黄疸患者围手术期易感性明显高于非黄疸者，发病原因尚不完全清楚。本文研究了阻塞性黄疸大鼠脾脏淋巴细胞白细胞介素２（ＩＬ－２）生成能力及抑制性Ｔ淋巴细胞（Ｔｓ）功能的变化以及消炎痛的作用。结果表明。胆管结扎大鼠脾脏淋巴细胞ＩＬ－２生成明显下降，Ｔｓ细胞活性明显增强；消炎痛治疗使阻塞性黄疸大鼠脾脏淋巴细胞ＩＬ－２生成能力增强和ＴＳ细胞活性下降。提示阻塞性黄疸宿主免疫功能异常，可能是其围手术期易感性增高的原因之一，消炎痛有可能成为改善阻塞性黄疽病人免疫功能，降低感染易感性的有价值药物之一。     

布洛芬对创伤大鼠免疫调节作用的研究

研究了创伤大鼠免疫功能变化及布洛芬对创伤大鼠的免疫调节作用.结果证明:腹部创伤大鼠脾脏淋巴细胞 DNA 合成能力明显下降,脾脏 NK 细胞活性亦明显受到抑制;应用布洛芬治疗能够明显地改善创伤大鼠脾淋巴细胞的 DNA 合成能力,恢复脾脏 NK 细胞的活性,布洛芬能够改善创伤机体的免疫功能,提高其抗感染能力。     

布洛芬对创伤大鼠免疫调节作用的研究

研究了创伤大鼠免疫功能变化及布洛芬对创伤大鼠的免疫调节作用.结果证明:腹部创伤大鼠脾脏淋巴细胞DNA 合成能力明显下降,脾脏NK 细胞活性亦明显受到抑制;应用布洛芬治疗能够明显地改善创伤大鼠脾淋巴细胞的DNA 合成能力,恢复脾脏NK 细胞的活性,布洛芬能够改善创伤机体的免疫功能,提高其抗感染能力。     

布络芬对阻塞性黄疸大鼠的免疫调节作用

研究阻塞性黄疸大鼠脾脏淋巴细胞白细胞介素２生成能力的变化及细胞内ｃＡＭＰ、ｃＧＭＰ浓度的改变．同时观察布络芬对其的影响。结果显示；胆管结扎大鼠脾脏淋巴细胞白细胞介素２生成能力明显下降，细胞内ｃＡＭＰ浓度下降．ｃＧＭＰ水平上升；应用布络芬治疗的胆管结扎大鼠脾脏淋巴细胞白细胞介素２生成能力明显增强．细胞内ＣＡＭＰ浓度回升．ｃＧＭＰ水平下降。布络芬能够明显改善阻塞性黄疸大鼠的免疫功能，有可能成为临床上调节阻塞性黄疸病人免疫、降低感染易感性有价值的药物之一。     

肝动脉化疗栓塞术前后血清sIL－2R水平和IL－2活性变化

分别应用双抗体夹心酶联免疫法（ＥＬＩＳＡ）和Ｔ淋巴母细胞微量培养法，对４５例中晚期肝癌患者行肝动脉化疗栓塞术（ＴＡＣＥ）前后血清可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）水平和白细胞介素－２活性（ＩＬ－２）进行检测，并与３０例健康献血员比较。结果治疗前原发性肝癌患者ｓＩＬ－２Ｒ水平明显高于对照组，ＩＬ－２活性明显低于对照组。ＴＡＣＥ术后ＳＩＬ－２Ｒ水平明显下降，ＩＬ－２活性明显回升。应用免疫调节剂组较未用组ｓＩＬ－２Ｒ下降和ＩＬ－２升高更显著。结果提示：ＴＡＣＥ能改善机体免疫功能，给予合理的过继免疫治疗能增强这种作用     

精氨酸对阻塞性黄疸大鼠 IL-1 及 IL-2 的影响

目的：观察精氨酸在病理状态下对免疫功能的调节作用；方法：建立大鼠阻塞性黄疸模型，采用胸腺细胞及ＣｏｎＡ激活的脾细胞增殖法检测阻塞性黄疸大鼠ＩＬ－１及ＩＬ－２的活性；结果：阻塞性黄疸大鼠ＬＰＳ诱导的腹腔巨噬细胞产生的ＩＬ－１及Ｔ细胞分泌的ＩＬ－２均降低，精氨酸（２．７ｇ·ｋｇ－１·ｄ－１×７ｄ，ｉｇ）能使上述改变恢复正常，且精氨酸在该剂量对正常及阻塞性黄疸大鼠的肝肾功能无明显影响；结论：精氨酸对阻塞性黄疸大鼠免疫功能的降低有上调作用。     

燃煤颗粒物对大鼠免疫功能的影响

以不同剂量燃煤颗粒经气管染毒大鼠,在不同时间检测大鼠有关免疫功能。结果表明,低剂量燃煤颗粒不影响大鼠免疫功能,高剂量燃煤颗粒不影响脾脏的免疫功能,而抑制肺有关淋巴结的淋巴细胞转化功能和白细胞介素-2活性,肺巨噬细胞Fc受体数和抗肿瘤细胞毒效应早期激活,后期抑制。     

尿毒症患者淋巴细胞产生IL—2能力及IL—2表达的初步探讨

测定３５例尿毒症患淋巴细胞产生白细胞介素－２（ＩＬ－２）的活性水平和淋巴细胞白细胞介素－２受体（ＩＬ－２Ｒ）的表达。与正常对照组比较发现，透析和未透析尿毒症患的淋巴细胞产生ＩＬ－２的活性水平均明显下降，激活前淋巴细胞ＩＬ－２Ｒ表达增多。尿毒症患经慢性维持性血液透析后，淋巴细胞产生ＩＬ－２的活性水平有一定提高。研究结果为改善尿毒症患的细胞免疫功能提供了实验依据。     

Chemically induced immunotoxicity in a medium-term multiorgan bioassay for carcinogenesis with Wistar rats

A variety of chemicals can adversely affect the immune system and influence tumor development. The modifying potential of chemical carcinogens on the lymphoid organs and cytokine production of rats submitted to a medium-term initiation-promotion bioassay for carcinogenesis was investigated. Male Wistar rats were sequentially initiated with N-nitrosodiethylamine (DEN), N-methyl-N-nitrosourea (MNU), N-butyl-N-(4hydroxybutyl)nitrosamine (BBN), dihydroxy-di-n-propylnitrosamine (DHPN), and 1,2-dimethylhydrazine (DMH) during 4 weeks. Two initiated groups received phenobarbital (PB) or 2-acetylaminofluorene (2-AAF) for 25 weeks and two noninitiated groups received only PB or 2-AAF. A nontreated group was used as control. Lymphohematopoietic organs, liver, kidneys, lung, intestines, and Zymbal's gland were removed for histological analysis. Interleukin (IL)-2, IL-12, interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), IL-10, and transforming growth factor beta1 (TGF-beta1) levels were determined by ELISA in spleen cell culture supernatants. At the fourth week, exposure to the initiating carcinogens resulted in cell depletion of the thymus, spleen and bone marrow, and impairment of IL-2, IL-12, and IFN-gamma production. However, at the 30th week, no important alterations were observed both in lymphoid organs and cytokine production in the different groups. The results indicate that the initiating carcinogens used in the present protocol exert toxic effects on the lymphoid organs and affect the production of cytokines at the initiation step of carcinogenesis. This early and reversible depression of the immune surveillance may contribute to the survival of initiated cells facilitating the development of future neoplasia.     

牛膝多糖的免疫调节作用

为深入探讨牛膝多糖(ABPS)对免疫系统的作用机制,用体内、外的方法,对老年鼠一些免疫功能进行了研究。研究表明,ABPS在体外可以提高老年小鼠T淋巴细胞的增殖能力和IL-2的分泌。体内能显著提高老年大鼠T淋巴细胞和血清中TNF-β或TNF-α及NO的产生和NOS的活性,降低其sIL-2R的产生;ABPS50～800mg·L^-1体外给药或100mg·kg^-1ip可提高老年大鼠PMΦTNF-α及NO的产生和NOS的活性,ABPS100mg·kg^-1ip并能提高LPS诱导的PMΦTNF-α及NO的产生和NOS的活性。ABPS对老年大鼠大脑皮层NO的产生及NOS的活性无影响。提示ABPS可以启动和活化MΦ,纠正老年鼠的免疫低下状态,是免疫调节剂。     

华支睾吸虫病患者细胞因子水平的测定及临床意义

目的:探讨华支睾吸虫病患者细胞因子水平的测定及临床意义.方法:用放射免疫法及双抗体夹心酶联免疫吸附测定(ELISA)法,检测40例华支睾吸虫病患者血清白细胞介素2(IL-2)和可溶性白细胞介素2受体(sIL-2R)并进行统计分析.结果: 华支睾吸虫病患者sIL-2R水平明显增高,与健康人对照组比较差异有显著性(P＜0.05),而IL-2含量明显减少,与健康人对照组比较差异有显著性(P＜0.01).结论:华支睾吸虫病患者细胞免疫功能降低.     

Estradiol-induced alteration in the immune system. II. Suppression of cellular immunity in the rat is not the result of direct estrogenic action

Estradiol has been reported to suppress numerous cellular immune response. What is not known is how estradiol exerts this effect. In vivo administration of estradiol to male rats caused time-related immunomodulatory effects leading to enhancement of lymphocyte transformation while suppressing a mixed lymphocyte reaction (MLR) response. The suppression of the MLR response was not due to alterations in the ratio of helper and suppressor T cells, nor was it due to alterations in either cell viability or the number of cells in culture. Lymphocytes cultured in vitro with estradiol, however, fail to show any alteration in the responsiveness in either MLR or lymphocyte transformation assays. The suppressive effects of estradiol cannot be transferred from a primary MLR culture to a second MLR culture using the supernatants from the primary MLR culture. Lymphocytes from animals given estradiol in vivo show no alteration in the production of interleukin 2: added in vitro to primary MLR cultures, Interleukin 2 failed to restore full responsiveness to lymphocytes from animals treated in vivo with estradiol. These results suggest that estradiol acts indirectly to cause an alteration in the responsiveness of the regulatory cells of the cellular immune system.     

Effect of adenosine receptor subtypes stimulation on mixed lymphocyte reaction

The cell-to-cell interaction through binding of intercellular adhesion molecule (ICAM)-1 on monocytes to their ligands lymphocyte function-associated antigen (LFA)-1 on T-cells plays important roles in cytokine production and T-cell proliferation. Interleukin (IL)-18, which plasma levels are elevated in patients during acute rejection following organ transplantation, induces the expression of ICAM-1 on monocytes, production of interferon (IFN)-gamma and IL-12 and lymphocyte proliferation during human mixed lymphocyte reaction. Activation of the adenosine A(2A) receptor on during reperfusion of various tissues has been found to markedly reduce ischemia-reperfusion injury. In the present study, we examined the effect of adenosine at increasing concentrations ranging from 0.1 to 100 microM on the IL-18-enhanced expression of ICAM-1, production of IFN-gamma and IL-12 and lymphocyte proliferation during human mixed lymphocyte reaction. Adenosine inhibited the IL-18-initiated immune responses. The IC(50) values of adenosine for inhibition of the IL-18-enhanced ICAM-1 expression, IFN-gamma production and lymphocyte proliferation were 20 microM, respectively. The actions of adenosine depended on the stimulation of adenosine A(2A) receptor. An inhibitor of protein kinase A (PKA) at 100 microM inhibited the actions of adenosine, suggesting that PKA might be involved in the actions of adenosine. On the other hand, the stimulation of adenosine A(1) and A(3) receptor blocked the actions of adenosine A(2A) receptor stimulation. These results suggest that adenosine inhibits the immune responses during mixed lymphocyte reaction via adenosine A(2A) receptor.     

Protective effect of nerve growth factor on neurons after traumatic brain injury

The protective effect of nerve growth factor (NGF) on neurons after traumatic brain injury (TBI) was investigated. A brain trauma model of fluid-percussion in rats was established, and 7s NGF was infused continuously in its cerebral ventricle. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and [Ca2+]i overloading in brain tissues was observed after giving exogenous NGF postinjury. We found that the activity of SOD, GSH-Px, and CAT was markedly higher in NGF-treated group than in the simple trauma group (P < 0.01). Although the level of [Ca2+]i in the NGF-treated group increased, the value was significantly lower than that in the simple trauma and control groups (P < 0.01). These findings suggest that exogenous NGF can (a) increase the activity of the major antioxidant enzymes in brain tissues and attenuate the injuries to neurons induced by oxygen-free radicals, (b) reduce the severe overload of [Ca2+]i and stabilize its homeostasis, and (c) provide clear protective effects on neurons after traumatic brain injury.     

虎杖提取物抗炎作用的实验研究

[目的]考察虎杖的乙酸乙酯提取物的抗炎作用及初步机制。[方法]分别以地塞米松、阿司匹林和环磷酰胺为阳性对照药,采用虎杖的乙酸乙酯提取物对小鼠和大鼠的多种炎症模型进行抑制实验。[结果]虎杖的乙酸乙酯提取物对角叉菜胶所致大鼠足跖肿胀有显著抑制作用(P<0.00 J);对小鼠、大鼠纸片法所致肉芽肿有显著抑制作用(P<0.01);对腹腔注射醋酸所致小鼠毛细血管通透性增高有显著抑制作用(P<0.01);对角叉菜胶所致小鼠肿胀足中炎症介质PGE2合成有显著抑制作用(P<0.001);对三硝基氯苯诱导的小鼠迟发性超敏反应有显著抑制作用(P<0.01);对肾上腺切除大鼠纸片法致肉芽肿(P<0.01)及角叉菜胶所致足跖肿胀(P<0.05)有显著抑制作用,但其抑制率均较正常大鼠相应实验抑制率有所降低。[结论]虎杖的乙酸乙酯提取物有一定的抗炎作用,其作用机制可能是抑制炎症介质PGE2的合成、抑制细胞免疫及与垂体-肾上腺皮质系统有关。