白芍总甙对正常人与类风湿性关节炎患者单核细胞和淋巴细胞功能的影响

０．１～２．５ｍｇ·Ｌ－１白芍总甙（ＴＧＰ）对正常人的ＬＰＳ诱导外周血单个核细胞产生ＩＬ－１．ＰＨＡ－Ｐ诱导淋巴细胞增殖反应和ＩＬ－２产生均呈现浓度依赖性的双向作用；ＴＧＰ还可浓度（０．１～１２．５ｍｇ·Ｌ－１）依赖性地降低正常人淋巴细胞上ＩＬ－２Ｒ的密度．ＴＧＰ能使类风湿性关节炎（ＲＡ）患者低下的ＰＨＡ－Ｐ致分裂素反应与ＩＬ－２产生能力恢复正常，使外周血中减少的Ｔｓ细胞数目回到正常水平．但可使ＲＡ患者ＰＢＭＣ过度产生ＩＬ－１降低至正常范围．并能显著降低ＲＡ患者增高的淋巴细胞ＩＬ－２Ｒ的密度。上述结果表明．ＴＧＰ对ＲＡ患者有明显的机能依赖性免疫调节作用．ＴＧＰ对ＲＡ的治疗作用可能与其调整ＲＡ患者异常的免疫功能有关。     

雷公藤治疗系统性红斑狼疮免疫机制的研究

目的：探讨雷公藤治疗系统性红斑狼疮的免疫作用机制。方法：用系统性红斑狼疮（ＳＬＥ）的外周血单个核细胞（ＰＢＭＣ）体外培养观察雷公藤对于ＳＬＥ的Ｔ,Ｂ细胞功能的影响。结果;雷公藤不仅能抑制ＳＬＥ病人ＰＢＭＣ对ＰＨＡ诱导的增殖反应,也能抑制ＳＬＥ病人活化Ｂ细胞的自发增殖以及ＳＡＣ诱导的静止期Ｂ细胞的增殖反应。另外雷公藤还能明显的抑制ＳＬＥ病人ＰＢＭＣ的自发性ＩｇＧ分泌以及ｒ－ＩＬ２诱导的ＰＢＭＣ的Ｉｇ     

黄芪多糖对烧伤小鼠细胞免疫功能的作用

应用小鼠烧伤模型，对黄芪多糖（ＡＰＳ）的免疫增强作用进行了体内外研究。结果表明：体内应用ＡＰＳ（２５０ｍｇ·ｋｇ－１，ｑｄ，连续５ｄ），可明显提高烧伤小鼠Ｔ淋巴细胞转化，ＩＬ－２的产生及ＩＬ－２Ｒ的表达；体外分别应用５０、１００、２５０ｍｇ·Ｌ－１的黄芪多糖，发现其可纠正烧伤小鼠Ｔ淋巴细胞转化，ＩＬ－２的产生及ＩＬ－２Ｒ表达的受抑状态，并促进巨噬细胞产生ＩＬ－１，抑制ＰＧＥ２合成，且呈剂量依赖关系；体外去除烧伤小鼠脾细胞中的巨噬细胞后，ＡＰＳ对Ｔ淋巴细胞转化，ＩＬ－２产生及ＩＬ－２Ｒ表达的调节作用消失。提示ＡＰＳ对烧伤小鼠的免疫调节作用依赖于巨噬细胞，通过调节其分泌ＩＬ－１，抑制ＰＧＥ２合成，而促进ＩＬ－２产生及ＩＬ－２Ｒ表达，进而增强Ｔ淋巴细胞增殖。     

再生障碍性贫血患者外周血单个核细胞产生某些细胞因子能力的变化及意义

观察再生障碍性贫血患者外周血单个核细胞（ＰＢＭＮＣ）产生 ＩＬ－１α、ＩＬ－２的能力及外周血清ｓＩＬ－２Ｒ水平,探讨这些变化的意义。方法：应用ＥＬＩＳＡ法测定细胞因子活性。结果〔显示再障患者ＰＢＭＮＣ产生ＩＬ－１α的能力明显低于对照组（Ｐ＜０．０１）;而产生 ＩＬ－２的能力则明显高于对照组（Ｐ＜０．０１）;血清 ｓＩＬ－２Ｒ水平明显高于对照组（Ｐ＜０．０１）。结论：这三项检测结果对于认识再障贫血的发病机制、辅助诊断疾病的严重程度、指导治疗和估计预后有一定意义。     

丹皮总苷体外对三类免疫细胞功能的影响

目的研究丹皮总苷（ＴＧＭ）体外对３类免疫细胞功能的影响。方法采用［３Ｈ］－ＴｄＲ参入法,检测Ｔ淋巴细胞增殖反应和分泌白介素２（ＩＬ－２）活性,Ｂ淋巴细胞增殖反应以及巨噬细胞产生ＩＬ－１。结果ＴＧＭ２～５０ｍｇ·Ｌ－１可明显促进刀豆蛋白Ａ诱导小鼠Ｔ淋巴细胞增殖反应和大鼠Ｔ淋巴细胞产生ＩＬ－２,ＴＧＭ还可促进脂多糖诱导Ｂ淋巴细胞增殖反应以及大鼠腹腔巨噬细胞产生ＩＬ－１,它们的浓度－效应曲线呈钟罩形。结论ＴＧＭ具有浓度依赖性双向免疫调节作用。     

再生障碍性贫血患者外周血单个核细胞产生某些细胞因子能力的变化？…

目的：观察再生障碍性贫血患者外周血单个核细胞（ＰＢＭＮＣ）产生ＩＬ－１α、ＩＬ－２的能力及外周血清ｓＩＬ－２Ｒ水平,探讨这些变化的意义。方法：应用ＥＬＩＳＡ法测定细胞因子活性。：显示再障患者ＰＢＭＮＣ产生ＩＬ－１α的能力明显低于对照组;而产生ＩＬ－２的能力则明显高于姐;血清ＳＩＬ－２水平明显高于对照组。结论：」这三项检测结果对于认识再障贫血的发病机制,辅助诊断疾病的严重程度、指导治疗和估计预后有一     

白芍总甙对B淋巴细胞增殖和白介素1生成的调节作用

白芍总甙（ＴＧＰ）对脂多糖（ＬＰＳ）诱导的小鼠脾淋巴细胞增殖反应的量效曲线呈钟形，用贴壁法除去脾细胞中巨噬细胞（ＭΦ）或加入１０μｍｏｌ·Ｌ１吲哚美辛（Ｉｎｄ）可使ＴＧＰ量效曲线的下降支消失，再加５％同系小鼠腹腔ＭΦ中或前列腺素Ｅ２（ＰＧＥ２）０．０２２０μｍｏｌ·Ｌ１可使量效曲线下降支再现．同步检测ＴＧＰ对ＬＰＳ诱导大鼠腹腔ＭΦ产生ＰＧＥ２与白介素１（ＩＬ１）．结果表明，ＴＧＰ０．５－３ｌ２．５μｇ·ｍＬ１对ＬＰＳ诱导的ＩＬ－１产生曲线呈钟形．而ＴＧＰＬＰＳ的ＰＧＥ２产生曲线呈浓度依赖性地增高；在１２．５－３１２．５μｇ·ｍＬＴＧＰ范围内，１０μｍｏｌ·Ｌ１Ｉｎｄ可使高浓度ＴＣＰＬＰＳ的ＩＬ－１释放曲线明显抬高。提示ＴＧＰ对ＬＰＳ诱导的Ｂ细胞增殖反应和ＩＬ－１诱生的负调节作用都与其促进ＭΦ释放ＰＧＥ２有关．     

IL-2-PE40对免疫活性T细胞的影响

目的研究ＩＬ－２－ＰＥ４０对免疫活性Ｔ细胞的影响。方法采用ＣｏｎＡ刺激的淋巴细胞增殖试验、混合淋巴细胞培养（ＭＬＣ）及细胞毒试验。结果ＩＬ－２－ＰＥ４０对ＣｏｎＡ诱导的小鼠脾细胞有十分强的细胞毒性，能选择性地抑制ＭＬＣ中抗原活化的Ｔ细胞活性，保留未活化Ｔ细胞对ＣｏｎＡ诱导的丝裂原反应，在培养ｄ３加入ＩＬ－２－ＰＥ４０比培养开始时加入对ＭＬＣ抑制作用强。结论ＩＬ－２－ＰＥ４０能够高度选择性抑制免疫活性Ｔ细胞，是ＩＬ－２Ｒ靶向治疗中具有潜力的一种免疫抑制剂。     

1α,25-二羟维生素D_3对患者PBMC分泌的IFN-α和IL-10水平的影响

目 的 探 讨 １α，２５－二羟 维生 素 Ｄ_３（１α，２５－（ＯＨ ）２Ｄ ）对 系 统性 红斑 狼 疮（ＳＬＥ）患 者 外周 血 单个 核 ３细 胞（ＰＢＭ Ｃ）分 泌的 白细 胞 介素 （ＩＬ）－１０ 和 干扰 素 （ＩＦＮ ）－α水平 的 影响 。方法 ２０ 例 ＳＬＥ 患 者和 １０ 名健 康 志愿者 ＰＢＭ Ｃ 的提 取 采 用 Ｆｉｃｏｌ密 度 梯 度 离 心 法 ，ＳＬＥ 组 和 对 照 组 在 不 加 或 加 入 １α，２５－（Ｏ Ｈ ）２Ｄ３ 的 情 况 下 孵 育 ７２ ｈ收 集培 养 上清 ，上 清液 ＩＬ－１０ 和 ＩＦＮ－α水平 检 测采 用酶 联 免疫 吸附 试 验（ＥＬＩＳＡ ）。结 果 与 正常 对 照组 相比 ，ＳＬＥ组 ＰＢＭ Ｃ 中 ＩＬ－１０ 和 ＩＦＮ－α水 平 明 显 增高 （Ｐ＜０．０１）。０．０１ ｍ ｏｌ／Ｌ １α，２５－（Ｏ Ｈ ）２Ｄ３ 的 加 入 明 显 抑 制 了 ＳＬＥ 组ＰＢＭ Ｃ 中 ＩＦＮ －α的 产 生 （Ｐ＜０．０１），增 加 了 ＳＬＥ 组 ＰＢＭ Ｃ 中 ＩＬ－１０ 的 产 生 （Ｐ＜０．０１），但 对 正 常 对 照 组 ＩＦＮ －α和ＩＬ－１０ 水平 无明 显 影响 。结 论 １α，２５－（ＯＨ ）２Ｄ 可 能 抑制 体外 培 养的 ＳＬＥ 患 者 ＰＢＭ Ｃ ＩＦＮ －α的产 生     

白细胞介素－1β诱导牛脑微血管平滑肌细胞增殖及药物的拮抗作用

研究白细胞介素－１β（ＩＬ－１β）对牛脑微血管平滑肌细胞（ＢＣＳＭＣ）增殖的影响。浓度为５～１００ｎｇ·Ｌ－１的ＩＬ－１β与ＢＣＳＭＣ共同孵育２４ｈ，即可明显诱导ＢＣＳＭＣ的增殖，ＩＬ－１β浓度为５０ｎｇ·Ｌ－１时，增殖率为１７％。欧芹素乙，异欧芹素乙，６－（α，α－二苯基乙酰哌嗪基苯基－４，５－二氢－５－甲基－３（２Ｈ）－哒嗪酮（简称ＤＭＤＰ），６－（α－本基乙酰哌嗪基苯基）－４，５－二氢－５－甲基－３（２Ｈ）－哒嗪酮（简称ＰＭＤＰ）分别在不同浓度可显著抑制ＩＬ－１β所诱导的ＢＣＳＭＣ增殖。     

系统性红斑狼疮患者外周血淋巴细胞增殖功能及其产生白细胞介素2的研究

目的　研究系统性红斑狼疮 (SLE)患者外周淋巴细胞 (PBL)增殖反应及其产生白细胞介素 2 (IL 2 )的情况。方法　淋巴细胞增殖法及IL 2检测法。结果　SLE患者PBL的增殖反应明显高于正常人 ,但SLE患者PBL产生IL 2的能力明显低于正常人。结论　SLE患者PBL增殖反应提高和其产生IL 2能力降低可能与T细胞两亚群TH1 /TH2 的失衡有关。     

甲硫氨酸脑啡肽对系统性红斑狼疮患者外周血淋巴细胞增殖反应的影响及阿片受体介导机制的研究

目的　研究甲硫氨酸脑啡肽 (Met Enk)对系统性红斑狼疮 (SLE)患者外周血淋巴细胞 (PBL)增殖反应的影响以及纳络酮 (Nal)对其影响的作用。方法　淋巴细胞增殖法。结果　Met Enk(1× 10 -8～ 1× 10 -6mol·L-1)能够促进正常人PBL增殖反应 ,Nal(1× 10 -6mol·L-1)对正常人PBL增殖反应无明显影响 ,但可拮抗Met Enk(1× 10 -6mol·L-1)对正常人PBL增殖反应的促进作用 ;Nal(1× 10 -6mol·L-1)不仅可拮抗Met Enk(1× 10 -6mol·L-1)对SLE患者PBL增殖反应的促进作用 ,而且可直接降低SLE患者PBL增殖反应。结论　内源性Met Enk通过阿片受体参与了SLE患者PBL功能的上调作用     

褪黑素对类风湿关节炎病人外周血淋巴细胞增殖反应的影响及其G蛋白-cAMP信号转导机制的研究

目的研究褪黑素（ＭＴ）对类风湿关节炎（ＲＡ）病人外周血淋巴细胞（ＰＢＬ）增殖反应的影响及其Ｇ蛋白 ｃＡＭＰ信号转导机制。方法淋巴细胞增殖法、ｃＡＭＰ放免测定及Ｇ蛋白功能分析。结果ＲＡ病人ＰＢＬ增殖能力低于正常人１０倍左右，ＭＴ在１×１０－８～１×１０－６ｍｏｌ·Ｌ－１能明显促进ＲＡ病人ＰＢＬ的增殖反应；ＲＡ病人ＰＢＬ的ｃＡＭＰ水平明显高于正常人，ＭＴ（１×１０－６ｍｏｌ·Ｌ－１）可部分使其降低，且ＭＴ的这一作用能被百日咳毒素（ＰＴ）取消。结论ＭＴ可促进ＲＡ病人ＰＢＬ的增殖反应，ＰＴ敏感的Ｇｉ蛋白 ｃＡＭＰ信号转导机制参与了ＭＴ上调ＰＢＬ的作用     

Decreased lymphocyte blastogenesis,IL2 production and NK activity following nifedipine administration to healthy humans

Summary The effects of a single oral dose of nifedipine on part of the immune response in healthy humans has been investigated in terms of two different immune functions: T lymphocyte proliferation and NK activity. Both functions are known to require calcium ions.Ten healthy subjects were bled before and 30 min, and 4 and 24 h after receiving 10 mg nifedipine. Lymphocyte proliferation, both in mitogen-activated lymphocyte cultures, and in autologous and allogeneic mixed lymphocyte reactions, was significantly reduced (up to 48%) 30 min after drug administration and reverted to normal 4 h later. The inhibition could be attributed to reduction in IL2 production by the T cells isolated 30 min following the administration of nifedipine, since they normally express IL2-receptors. The addition of recombinant IL2 of 200 U·ml^–1 to the cell cultures restored their responsiveness.NK activity was significantly reduced 30 min and 4 h after drug administration and returned to normal at the 24th h. This function was also restored by the addition of IL2.The data suggest that calcium channel blockers may inhibit, at least transiently, lymphocyte functions in vivo.List of abbreviations AMLC Autologous mixed lymphocyte cultures - CD Cluster determinants - ConA Concanavallin A - CTL Cytotoxic T lymphocytes - GAM-FITC Fluorescein isothiocyanate-conjugated goat anti-mouse immunoglobulins - HLA-class II DP-DQ-DR antigens - IL2 Interleukin 2 - mAb Monoclonal antibodies - MHC Major histocompatibility gene complex - MLC Mixed lymphocyte cultures - NK Natural killer activity - non- T/T type AMLC Autologous mixed lymphocyte culture in which non-T cells are used as stimulators - PBL Peripheral blood lymphocytes - T/T type AMLC Autologous mixed lymphocyte culture in which PHA-activated T lymphocytes are used as stimulators     

组胺对细胞免疫反应调节作用的实验研究

目的　了解组胺对 CD4和 CD8T细胞白细胞介素 - 2 (IL- 2 )产生和细胞增生活性的影响。方法　密度梯度离心及吸附法分离外周血单个核细胞 (PBMC)和外周血淋巴细胞计数 (PBL C) ,采用抗 CD4和抗 CD8抗体分别制备 CD8和 CD4T细胞进行培养 ,然后采用酶联免疫吸附法 (EL ISA法 )和四氮唑蓝快速比色法(MTT)测上清液 IL - 2含量及增生活性。结果　 1组胺 +CD4(CD8)培养上清液中 IL - 2水平及 MTT增生指数与T细胞自然培养孔比较明显降低 (P<0 .0 5 )。 2组胺 +CD4(CD8) +西咪替丁培养孔上清液中 IL - 2水平及 MTT增生指数明显高于未加西咪替丁孔 (P<0 .0 5 )。 3 CD4T细胞自然培养孔上清液中 IL- 2水平显著高于 CD8T细胞自然培养孔。结论　 1组胺可抑制 T细胞 IL- 2产生及增生 ;2西咪替丁可阻断组胺对 T细胞的抑制作用 ;3CD8T细胞也可产生 IL- 2 ,但其功能较 CD4T细胞为低     

白芍总苷对小鼠系统性红斑狼疮样改变的保护作用

目的　观察白芍总苷 (TGP)对空肠弯曲菌CJ S13 1诱导的小鼠SLE样改变的保护作用。方法　采用空肠弯曲菌CJ S13 1和CFA混合免疫动物 ,诱导小鼠SLE样改变。结果　TGP 5 0 ,10 0 ,2 0 0mg·kg-1·d-1× 2 8d ,ig能部分或完全拮抗血清IgG型自身抗体水平的升高 ,抑制ConA及LPS诱导的淋巴细胞增殖反应的增强和IL 1生成的增多。结论　一定剂量的TGP对小鼠SLE样改变具有一定的保护作用     

Defect in regulation of Ca2+ movement in platelets from patients with systemic lupus erythematosus

The differences in the intracellular Ca(2+) responses to hormones in platelets from systemic lupus erythematosus (SLE) patients compared to normal humans have not been explored. This study examined the Ca(2+) signaling and density of platelets in normal, inactive and active SLE patients. The platelet number per mul in inactive and normal groups did not differ, whereas the number in active SLE patients was smaller than the other two groups by 60%. The intracellular free Ca(2+) levels ([Ca(2+)](i)) in response to stimulation of four endogenous Ca(2+) mobilizing hormones, 100 microM arachidonic acid (AA), 10 microM ADP, 10 nM platelet activation factor (PAF) and 1 microM thrombin, were investigated using the Ca(2+)-sensitive fluorescent dye, fura-2. The AA-induced [Ca(2+)](i) rises in normal and inactive groups were similar. In contrast, the AA-induced [Ca(2+)](i) rises in the active SLE group were significantly smaller than in the normal and inactive groups. The defect in the AA-induced [Ca(2+)](i) rises in active SLE groups appears to be caused by defective Ca(2+) influx and Ca(2+) releasing pathways because the AA-induced responses were not altered by removal of extracellular Ca(2+), whereas the AA-induced responses in normal and inactive SLE groups were reduced by removal of extracellular Ca(2+), and the AA-induced Ca(2+) release was smaller in the active SLE group. PAF, ADP and thrombin all induced [Ca(2+)](i) rises in the three groups, but no significant differences were found among the three groups. Together, the results indicate that cell density and Ca(2+) signaling in platelets from active SLE patients are altered in response to particular stimulators. In these regards, platelets from inactive SLE patients appear to be similar to those from normal humans.     

Immunoregulatory abnormalities of T cells and hyperreactivity of B cells in the<Emphasis Type="Italic">In Vitro</Emphasis> immune response in pristane-induced lupus mice

Systemic lupus erythematosus (SLE) is characterized by overactive B cells that differentiate into autoantibody-forming cells, aberrant T cell function that provides helping B cells produce autoantibodies, and overproduction of proinflammatory cytokines. However, immunodysregulation in lupus pathogenensis remains incomplete. We examined mitogen-stimulated production of proinflammatory cytokines, cell proliferation, T cell activation, and T cell apoptosis in vitro in pristane-induced lupus BALB/c mice compared to normal mice. LPS-stimulated production of IL-6 and IL-10 by splenocytes and macrophages from pristane-induced lupus mice were remarkably up-regulated compared to normal mice, whereas production of macrophage TNF-alpha was significantly down-regulated. Moreover, in vitro production of IL-2, IL-6, IL-10 and IFN-gamma by Con A-stimulated splenocytes, cell proliferation in LPS- or Con A-stimulated- thymocytes and splenocytes, and expression of CD69+CD4+ T cells in Con A-stimulated splenocytes were greatly increased in cells derived from pristane-induced lupus mice compared to normal mice. In addition, splenic T cells and CD4+ T cells in thymocytes from pristane-induced lupus mice were more resistant than nonautoimmune normal cells to Con A-induced apoptosis. Our findings indicate that immunoregulatory abnormalities of T cells and hyperreactivity of B cells in the in vitro immune responses in pristane-induced lupus mice may explain some of lupus pathogenesis.