青蒿琥酯及其与放疗联用对CNE细胞的作用

目的研究青蒿琥酯及其与放疗联用对鼻咽癌CNE细胞增殖和凋亡的影响。方法采用细胞集落计数法和原位末端标记（TUNEL）法,测定单用青蒿琥酯及其与放疗联用对CNE细胞增殖的抑制作用和对凋亡的诱导。结果青蒿琥酯能够抑制CNE细胞增殖,并呈现明显的剂量效应,药物浓度2．5～50μg／ml的细胞存活率为15．75％～93．64％。青蒿琥酯可诱导CNE细胞凋亡,高浓度组（10μg／ml）作用比低浓度组（5μg／ml）强（P〈0．05）。当青蒿琥酯与放疗联用时作用更为明显,联用组的作用效果均优于单用青蒿琥酯组或单纯放疗组。结论青蒿琥酯对CNE细胞增殖有明显的抑制和诱导凋亡作用,且和放疗联用作用更强。     

黄芪多糖对兔脂肪来源的间充质干细胞体外增殖的影响

目的黄芪多糖(APS)对兔脂肪来源的间充质干细胞(ASCs)体外增殖的作用。方法提取兔ASCs进行培养,设实验组和对照组,实验组加入不同浓度APS注射液,对照组加常规培养液,四甲基偶氮唑盐(MTT)法观察细胞的增殖率,比较两组之间的差异。结果 APS浓度为1.95～3.90μg/mL时,对ASCs的增殖无明显影响(P>0.05);而浓度为7.80～1 000μg/mL时,对ASCs的增殖有明显抑制作用(P<0.01);在一定浓度范围内(25～100μg/mL),浓度对细胞增殖的影响不大,而与培养的时间有关,随着作用时间的延长,对ASCs的抑制作用更加明显。结论低浓度APS对兔ASCs体外增殖无影响;高浓度APS对ASCs有明显的抑制作用。     

饥饿对小鼠免疫功能的影响

目的研究饥饿对小鼠非特异性免疫和特异性免疫功能的影响。方法根据小鼠进食量的75％、50％、25％、100％分成高、中、低剂量及空白对照组,根据小鼠进食量计算出100％进食组每日进食量约为0．4g／只,高、中、低剂量组分别为0．3g／只、0．2g／只、0．1g／只,连续喂养10d后,测定各组小鼠的体重、胸腺和脾脏重量,计算胸脾指数;检测中性粒细胞的吞噬率、T淋巴细胞Ea花环形成率。结果与对照组比较,高、中、低剂量组的小鼠的体重、胸腺及脾脏指数明显降低（P〈0．05）。结论饥饿能够影响小鼠非特异性免疫功能。     

海参提取物对免疫功能低下模型小鼠免疫功能的调节作用

目的:研究海参提取物对免疫功能低下模型小鼠免疫功能的调节作用。方法:50只ICR小鼠随机均分为正常对照(等容生理氯化钠溶液)组、模型(等容生理氯化钠溶液)组、左旋咪唑(40 mg/kg)组与海参提取物高、低剂量[500、250 mg(生药)/kg]组,灌胃给药,每天1次,连续10 d。给药7 d后,腹腔注射环磷酰胺(40 mg/kg),每天1次,连续3 d以复制小鼠免疫功能低下模型。小鼠尾静脉注射0.5%刚果红溶液(0.1 ml/10 g),采血,分光光度计测定其光密度以评价单核巨噬细胞吞噬能力;细胞计数仪读取白细胞数;酶联免疫吸附(ELISA)法检测血清免疫球蛋白(Ig)G水平;称定小鼠胸腺、脾脏与体质量以计算免疫脏器指数;2(-2-甲氧基-4-硝基苯基)-3-(4-硝基苯基)-5-(2,4-二磺酸苯)-2H-四唑单钠盐(CCK-8)法检测淋巴细胞增殖能力。结果:与正常对照组比较,模型组小鼠吞噬指数(κ)、校正吞噬指数(α)差异无统计学意义(P>0.05);白细胞数减少,血清Ig G含量减少,胸腺指数、脾脏指数降低,脂多糖(LPS)刺激增殖率、刀豆蛋白A(Con A)刺激增殖率降低,差异均有统计学意义(P<0.01)。与模型组比较,海参提取物高、低剂量组小鼠α升高,血清Ig G含量增加;海参提取物高剂量组κ升高、白细胞数增加,差异均有统计学意义(P<0.01或P<0.05);海参提取物高、低剂量组胸腺指数、脾脏指数、LPS刺激增殖率、Con A刺激增殖率差异无统计学意义(P>0.05)。结论:海参提取物对化疗药物环磷酰胺所致小鼠免疫功能低下具有一定的调节改善作用。该研究为海参调节免疫功能的临床应用提供了实验依据。     

鸡枞菌多糖对免疫抑制小鼠免疫功能的影响

目的探讨鸡枞菌多糖(TAP)对环磷酰胺所致免疫抑制小鼠免疫功能的影响。方法以黄芪多糖(APS)为阳性对照,用不同剂量的TAP对免疫抑制小鼠进行腹腔注射,检测其腹腔巨噬细胞吞噬功能,免疫器官指数、血清溶血素、T淋巴细胞亚群、细胞因子、脾淋巴细胞增殖等免疫指标。结果 TAP在5～20 g.L-1浓度范围内不同程度增强巨噬细胞吞噬功能及提高免疫器官指数,且有剂量依赖性;20 g.L-1TAP可明显降低免疫低下小鼠CD4+/CD8+比值,并使IL-2、IFN-γ水平分别上升312.3%和88.1%,同时降低IL-4水平;TAP能明显提高脾淋巴细胞增殖能力。结论 TAP可提高免疫抑制小鼠体液及细胞免疫功能,且效果优于APS。     

黄芪多糖对MIN6细胞增殖、凋亡及胰岛素分泌的影响

目的:研究不同浓度黄芪多糖(Astragalus polysaccharide,APS)对胰岛MIN6细胞的增殖活性、细胞凋亡及胰岛分泌功能的影响。方法:用不同浓度APS(0,10,100和1 000μg.mL-1)干预MIN6细胞48 h,采用MTT法测细胞增殖活性,流式细胞仪检测细胞凋亡,分别用3和30 mmol.L-1葡萄糖刺激各组MIN6细胞,胰岛素放免试剂盒检测胰岛素分泌功能。结果:与对照组(0μg.mL-1)比较,100μg.mL-1 APS组MIN6细胞增殖活性升高(P<0.05);10和100μg.mL-1 APS组MIN6细胞凋亡率有下降趋势,而1 000μg.mL-1 APS组MIN6细胞凋亡率明显增加(P<0.05);10和100μg.mL-1 APS组MIN6细胞胰岛素分泌功能显著增强(P<0.05),而1 000μg.mL-1 APS组MIN6细胞胰岛素分泌功能有下降趋势。结论:10和100μg.mL-1 APS使MIN6细胞增殖活性升高、细胞凋亡率下降以及胰岛素分泌功能升高;1 000μg.mL-1 APS使MIN6细胞增殖活性下降、细胞凋亡率升高及胰岛素分泌功能下降。     

白花蛇舌草提取物的体外抗肿瘤活性

目的 探讨白花蛇舌草乙醇提取物(SCD)的体外抗肿瘤活性。方法 以MTT法测定SCD对体外培养的肿瘤细胞增殖的抑制作用、对人外周血单个核细胞的增殖促进作用及增强自然杀伤细胞杀伤肿瘤细胞的作用。结果 100μg／ml SCD对KB、BGC、B16、HBL-60、SMMC-7721、HELA、A549的增殖仰制率分别为30．53％、42．82％、23．77％、63．93％、39．40％、46．33％、42．56％；250μg／ml SCD可促进PBMC增殖97．33％；联合Con A或者LPS作用时，在0．25μg／ml的低浓度下增殖率分别达344．13％和152．18％；高浓度SCD未明显增强NK的杀伤作用。结论 SCD对体外培养的肿瘤细胞有明显的抑制作用，SCD可以显著促进PBMC增殖。     

固相萃取-HPLC法快速测定苯妥英钠及卡马西平的血药浓度

目的 应用固相萃取(SPE)-反相HPLC法同时测定苯妥英钠(PHT)及卡马西平(CBZ)血药浓度。方法 将1ml血浆样品在GDX-403固相萃取柱上进行固相萃取，洗脱液混匀后直接进样。色谱条件：色谱：Hypersil BDS C18柱，流动相：甲醇：水=48：52，检测波长：235nm，流速：1ml／min，柱温：25℃，内标：非那西丁。结果 PHT在4．10-41．0μg／ml范围内线性良好(γ=0．9999)；CBZ在2．50-24．96μg／ml范围内线性良好（γ=0.9998)，方法平均回收率各为101.77％和101．87％，日内及日间误差分别小于4．13%和49.8％，最低检测浓度为：1．025μg／ml和0．156μg/ml。结论 该方法、准确、快速，可用于PHT及CBZ血浆浓度的同时测定。     

金银花多糖对脾淋巴细胞的增殖作用

目的研究金银花多糖对脾淋巴细胞的增殖作用。方法用MTT法体外观察金银花多糖在不同浓度对小鼠脾淋巴细胞增殖的影响。结果金银花多糖在浓度10～250μg／ml时可显著促进小鼠脾淋巴细胞的增殖,以浓度100μg／ml时作用最为明显。结论金银花多糖体外具有免疫促进作用。     

氟酰褪黑素对免疫功能低下小鼠免疫功能的影响

目的探讨免疫调节剂氟酰褪黑素{N-[2-(5-methoxy-2-ethoxycarbonyl-1H-indol-3-yl)-eth-yl]trifluoroacetamide,TFMMT}对免疫低下小鼠免疫功能调节作用。方法使用环磷酰胺(cy-clophosphamide,CY)致免疫低下动物模型,通过脾巨噬细胞吞噬功能、脾细胞悬液NK细胞活性、淋巴细胞转化实验、白介素-2(IL-2)的生成及脾上清中抗体水平测定,探索TFMMT对免疫低下小鼠免疫功能的影响。结果在CY所致的免疫低下动物模型中,TFMMT各剂量组能够完全对抗CY引起的吞噬能力下降,增强NK细胞活性;TFMMT高剂量组能显著保护CY引起的小鼠脾上清中抗体水平降低;在1.17×10-9～3.49×10-6mol.L-1浓度内,TFMMT剂量依赖性促进淋巴细胞转化功能,使免疫抑制小鼠脾脏中T淋巴细胞对ConA的反应显著提高;TFMMT可使免疫抑制小鼠脾细胞分泌IL-2水平升高,随剂量不断增大,作用反而减弱,呈剂量依赖性,但以在浓度为1.17×10-9～6.98×10-7mol.L-1内为显著。结论 TFMMT能较好保护CY所致的免疫低下小鼠的免疫功能。     

Different cellular responses of dexmedetomidine at infected site and peripheral blood of emdotoxemic BALB/c mice

Various sedative agents, including dexmedetomidine (dex), induce immunosuppression, and enhance infection progression. However, there was no information on how anesthetic affects local and systemic cellular immune function. We conducted this study to examine the impact of dex on the differentiation and function of immune cells at site of inflammation and in peripheral blood during endotoxemia of mice. In BALB/c mice with and without endotoxemia, we evaluated the influence of two dosages of 5 and 50 mcg/kg/h intravenous dex on immune cells: including number of T cells (CD3), B cells (CD19), natural killer cells (CD8a), monocytes (CD11b), and macrophages (Mac‐3) in peripheral blood, the activities of macrophages in peripheral blood and in peritoneal lavage, and proliferation of B and T cells and of natural killer cells activity in the spleen. Endotoxemia increased the number of CD3 T cells, CD 19 B cells and macrophages in the peripheral blood, augmented macrophage activity in the peritoneum, and increased T cell proliferation and natural killer cell activity in the spleen. Further administration of 5 mcg/kg/h dex attenuated systemic increase in number of T cells, B cells, and macrophages during endotoxemia and 50 mcg/kg/h dex significantly attenuated the increase in activity of macrophages in the peripheral blood during endotoxemia. In the peritoneum, however, 5 mcg/kg/h dex preserved and 50 mcg/kg/h dexmedetomidine enhanced the activity of macrophages during endotoxemia. Increased in proliferation of T cells in spleen during endotoxemia was attenuated by both doses of dex. Last, 50 mcg/kg/h dex enhanced natural killer cells activity during endotoxemia. While preserving the effects of endotoxemia on macrophage's activity in the infection site and natural killer cell's activity in the spleen, dex decreased systemic fulminant immune reaction in endotoxemia, by attenuating the augmented response in the number of T cells, B cells and macrophages, activity of macrophages in the peripheral blood, and proliferation of T cells in spleen during endotoxemia. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1416–1422, 2015.     

黄芩苷对化疗药物所致小鼠免疫低下的调节作用

目的研究黄芩苷对化疗药物所致小鼠免疫功能低下的调节作用。方法建立小鼠免疫低下模型,ig给予黄芩苷40,20,10 mg/kg,用流式细胞仪测定小鼠外周血中T淋巴细胞CD4+、CD8+亚群的分布,常规计数骨髓有核细胞数量,观察巨噬细胞吞噬指数、免疫器官脏器指数及组织形态的变化。结果黄芩苷能够提升免疫低下小鼠外周血T淋巴细胞亚群的水平,提高免疫功能,并改善化疗药物导致骨髓造血功能低下的不良反应。结论黄芩苷对化疗所致的免疫低下有保护作用,并能调节机体的免疫功能。     

Immunomodulatory activity of polysaccharide from Acanthopanax obovatus roots.

The effects of the Acanthopanax obovatus polysaccharide (AOPS) as well as its combination with cyclophosphamide (CY) or prednisolone on immune responses were investigated in mice. AOPS (250 mg/kg i.p. x 5) increased the spleen weight and the number of spleen cells, and augmented the phagocytosis of peritoneal macrophages both in normal mice and in immunosuppressed mice. In a haemagglutinin assay AOPS increased the production of specific antibodies and antagonized the suppressive effect of CY. AOPS not only enhanced the degree of in vitro spleen cell-mediated red blood cells (SRBC) hemolysis (quantitative hemolysis of SRBC) but also restored the suppressive effect of CY completely. From these results, AOPS was shown to have an enhancing and a modulating activity on immune responses.     

淫羊藿多糖对免疫功能低下小鼠免疫功能的影响

采用环磷酰胺所致免疫低下小鼠及荷瘤 (S180 )小鼠观察了淫羊藿多糖 (EPS)对免疫功能的影响 .结果表明 :腹腔注射环磷酰胺 80mg/kg ,可以使正常小鼠的胸腺指数、血清溶血素水平、空斑形成细胞溶血能力和外周血中WBC总数下降 .腹腔注射EPS 5 0、2 5mg/kg× 7,可使脾指数上升 ,但对胸腺指数无明显影响 ;5 0、2 5、12 5mg/kg× 7,使下降的溶血素值及空斑形成细胞的溶血能力回升 ;2 5、12 5mg/kg× 7,使下降的白细胞总数上升 .小鼠荷瘤后免疫功能低下 ,表现为胸腺指数下降、血清溶血素水平、空斑形成细胞的溶血能力及迟发性超敏反应能力降低 .皮下注射EPS5 0mg/kg× 8,可对抗荷瘤引起的胸腺指数下降 ;5 0、2 5mg/kg使荷瘤小鼠的脾指数升高 ;5 0、2 5mg/kg× 8,可以使荷瘤小鼠的血清溶血素、空斑形成细胞的溶血能力及迟发性超敏反应能力有所提高 .     

Immunomodulatory activity of resveratrol: discrepant in vitro and in vivo immunological effects

trans-Resveratrol is a dietary polyphenolic compound present in grapes, which has been shown to exhibit strong anti-inflammatory, antioxidant, and chemopreventive activities. In this study we have compared the in vitro and in vivo effects of resveratrol on the development of various cell-mediated immune responses, including mitogen/antigen-induced T cell proliferation, induction of cytotoxic T lymphocytes (CTLs), interleukin-2 (IL-2) induced lymphokine activated killer cells, and cytokine production. We found significant suppression (>90%) of the mitogen/antigen-induced T cell proliferation and development of allo-antigen specific CTLs in vitro with resveratrol at a concentration of 25 microM. Intragastric administration of resveratrol (2 mg daily) to mice for 4 weeks showed no effect on age-related gain in body weight, peripheral blood cell counts (WBC, RBC, or platelets), or the cellularity of bone marrow or spleen. The CD4(+) and CD8(+) T cells in spleen or colony-forming units-total in the marrow also remained unaffected by treatment with resveratrol. Spleen cells, which were stimulated in vitro after being removed from mice which had been administered resveratrol for 2 or 4 weeks, showed no significant change in IL-2 or concanavalin A induced proliferation of T cells or production of IL-2 induced lymphokine activated killer cells. Further, the production of in interferon-gamma and IL-12 was not affected by administration of resveratrol, but production of tumor necrosis factor-alpha was reduced. Even when conducted entirely in vivo, treatment with resveratrol was found to only marginally reduce allo-antigen induced T cell proliferation and the generation of CTLs in the draining lymph nodes. Thus, even though resveratrol strongly inhibits T cell proliferation and production of cytolytic cells in vitro, oral administration of resveratrol for 4 weeks does not induce hematologic or hematopoietic toxicity, and only marginally reduces the T cell-mediated immune responses.     

愈疡胶囊对正常小鼠外周血和脾T淋巴细胞亚群的影响

目的：研究愈疡胶囊对正常小鼠外周血和脾T淋巴细胞亚群的影响.方法：24只雄性昆明小鼠,随机分为正常对照组、阳性对照组、愈疡胶囊高剂量组和愈疡胶囊低剂量组 分别灌胃蒸馏水及相应药物,流式细胞仪测定外周血和脾淋巴细胞T淋巴细胞亚群.结果：与正常对照组比较,给药组能明显升高小鼠外周血和脾淋巴细胞T淋巴细胞亚群CD4分子表达量（P〈0.01或P〈0.001）.结论：愈疡胶囊可增强正常小鼠的细胞免疫功能,为该药的免疫增强作用提供了实验依据.     

复方党参口服液的免疫增强功能研究

目的：研究复方党参口服液对环磷酰胺所致免疫低下小鼠免疫功能的影响。方法：昆明种小鼠240只,分为4批,每批60只。每批小鼠随机分为空白组、模型组、阳性药物组、复方党参口服液高、中、低剂量组,每组10只,各组均连续灌胃4周,小鼠于给药3周后开始腹腔注射环磷酰胺40 mg·kg^-1,每天1次,连续2 d,建立小鼠免疫力低下模型;通过碳粒廓清试验、迟发型变态反应试验、脾淋巴细胞增殖转化试验、外周血白细胞计数、免疫器官指数五项相关免疫学指标,综合评价复方党参口服液对免疫低下小鼠免疫功能的调节作用。结果：与模型组比较,复方党参口服液可显著提高免疫功能低下小鼠的碳廓清吞噬指数、增强小鼠的迟发型变态反应的DTH程度;对抗环磷酰胺所致的小鼠外周血白细胞数、胸腺指数、脾脏指数以及脾淋巴细胞增殖转化能力的降低,显示出该制剂对免疫低下小鼠单核-巨噬细胞功能、细胞免疫功能的增强作用。结论：复方党参口服液可显著增强免疫低下小鼠的免疫功能,对免疫失衡机体具有一定的调节作用。     

The in vitro exposure to cypermethrin does not inhibit the proliferative response of peripheral blood mononuclear cells

This study evaluated the effect of in vitro exposure to cypermethrin on peripheral blood mononuclear cells proliferative response, considering reduced peripheral blood mononuclear cells proliferative response observed in individuals occupationally exposed to pyrethroids. Peripheral blood mononuclear cells were obtained from 21 healthy subjects (28.0?±?9.0 years old). The effect of cypermethrin (at 0.5, 1.0 and 5.0?mg/ml) on cell viability was evaluated by flow cytometry using an apoptosis detection kit. Cell proliferation (PI) was evaluated by 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE) fluorescence decay using flow cytometry. Cells labeled with CFSE were exposed, in vitro, to cypermethrin (0.5, 1.0, 2.0, 2.5 and 4?μg/ml) and stimulated with phytohemagglutinin (PHA 1.0 or 5.0?μg/ml) for 5?d (37?°C, 5% CO₂). The in vitro treatment of peripheral blood mononuclear cells with cypermethrin did not induce apoptosis or necrosis after 5?d in culture. Stimulation by PHA induced cell proliferation (PI?=?1.29?±?1.09 and 2.01?±?0.62, PHA at 1.0 and 5.0?μg/ml, respectively, mean?±?SD) and in vitro exposure to cypermethrin did not alter cellular proliferative response to PHA (PI?=?1.80?±?0.50, 2.60?±?0.05 and 2.10?±?1.20 for cypermethrin at 1.0, 2.0 and 4.0?μg/ml, respectively, and PHA at 5.0?μg/ml). In vitro treatment of peripheral blood mononuclear cells with cypermethrin, at the doses tested, does not affect cell viability or proliferation. These findings suggest that the reduction of proliferation observed on lymphocytes derived from individuals occupationally exposed to pesticides may be related to other mechanisms than direct action of cypermethrin on lymphocytes.     

Accelerated recovery from cyclophosphamide-induced leukopenia in mice administered a Japanese ethical herbal drug, Hochu-ekki-to

The effect of a Japanese ethical herbal drug, Hochu-ekki-to (HOT), on recovery from leukopenia induced by cyclophosphamide (CY) was investigated. Daily oral administration of 1000 mg/kg HOT into CY-treated mice significantly prevented decrease of leukocyte numbers in the peripheral blood and accelerated recovery from leukopenia. Ginsenoside Rgl extracted from Ginseng radix, a major herb of HOT, was one of the active ingredients. HOT increased numbers of neutrophils and monocytes in the peripheral blood compared with CY-treated control. Moreover, HOT augmented the resistance against Pseudomonas aeruginosa infection. The number of colony-forming units in the spleen (CFU-S) also increased in HOT-treated mice. The frequencies of IL-3-, GM-CSF- and IFN-gamma-producing cells increased in the spleen, bone marrow, liver and IEL on HOT treatment, and HOT clearly augmented the expressions of IL-3, GM-CSF and IFN-gamma mRNA in the spleen, bone marrow, liver and IEL except IL-3 and IFN-gamma mRNA in the IEL. These results suggest that HOT enhances the production of hematopoietic lymphokines, stimulates the proliferation of hematopoietic progenitor cells and consequently accelerates recovery from leukopenia in CY-treated mice. Additionally, IFN-gamma which HOT-augmented the production may contribute the protective effect against the bacterial infection by activating of phagocyte cells.     

Effects of methionine enkephalin on immune enhancement by reducing myeloid derived suppressor cells and reprogramming liver metabolism in colon cancer mice

OBJECTIVE To investigate enhanced immune function of methionine encephalin(MENK)and its anti-tumor mechanism in CT26 colon cancer mouse model.METHODS 3×10~6CT26 cells were implanted subcutaneously in BALB/c mice.Four days after,MENK was peritoneally administrated at the concentration of 20 mg·kg~(-1) for 14 d.The percentage of MDSCs in bone marrow,spleen,blood,tumor and liver were detected by flow cytometry.Non-esterified fatty acid(NEFA),triglycerides(TG)and total cholesterol(T-CHO)in liver homogenate were tested by a NEFA test kit,a TG test kit and a T-CHO test kit respectively.qRT-PCR and Western blot were used to measure m RNA and protein levels of inflammation-,glycometabolsim-and lipometabolsim-associated indexes in liver.RESULTS MENK decreased percentages of MDSCs in bone marrow,spleen,blood and tumor in colon cancer mice.MENK-treated mice displayed elevated ratio of CD4~+T and CD8~+T cells in spleen as well as increased T and B lymphocytes proliferation.Meanwhile,MENK also ameliorated liver damage reflected by lower levels of GPT and GOT in serum and reduced risks of cancer-associated index including inflammation,high lipid and high glucose.Furthermore,MENK lowered down the levels of NEFA,TG and T-CHO in liver homogenate.MENK treatment decreased expression of p-STAT3,increased expression of p-AKT,IRS1 and Glut4 at protein level as well as reduced lipogenesis-associated genes and elevated glycolysis-associated genes in liver of tumor bearing mice.Also,abated expression of genes associated with MDSCs generation(M-CSF,GM-CSF,IL-6,IL~(-1)β)and migration(S100A9,KC)was observed within shrunken subcutaneous tumor by MENK intervention.CONCLUSION MENK has the ability to strength immune function against colon cancer by reducing MDSCs and improving liver metabolism.