滨蒿提取物对环磷酰胺致小鼠免疫抑制的调节作用

目的 研究滨蒿提取物（Artemisia scopariaextract, ASE）对环磷酰胺诱导的免疫抑制小鼠免疫功能的影响。方法 采用腹腔注射环磷酰胺制备免疫抑制小鼠模型,称重法测定各组小鼠体质量、免疫器官脏器质量;碳粒廓清法检测小鼠巨噬细胞吞噬功能;MTS法检测小鼠脾T、B淋巴细胞增殖能力;ELISA法检测小鼠血清中肿瘤坏死因子-α(TNF-α)、γ-干扰素（IFN-γ）和免疫球蛋白M(IgM)的含量,综合评价滨蒿提取物对免疫抑制小鼠免疫功能的调节作用。结果 与空白对照组比较,模型组小鼠体质量、脾脏指数、胸腺指数、碳廓清指数（K）、吞噬指数（α）、脾淋巴细胞增殖能力及血清中TNF-α、IFN-γ和IgM的分泌均明显降低（P<0.05, P<0.01）,表明免疫抑制小鼠模型建立成功。与模型组比较,滨蒿提取物高剂量组可以显著提高免疫抑制小鼠胸腺指数,升高小鼠的α值,促进脾淋巴细胞增殖,增加免疫抑制小鼠血清中TNF-α的含量（P<0.05, P<0.01）;滨蒿提取物中、高剂量组均能显著升高免疫抑制小鼠的K值,促进小鼠血清中IFN-γ和IgM的分泌（P<0...     

牡蛎提取物对小鼠免疫功能的正向调节作用

牡蛎提取物连续胃饲小鼠１５ｄ（１０～３ｍｇ／ｄ），发现Ｔ细胞和Ｔｈ亚群百分比、ＣｏｎＡ和ＬＰＳ诱发的淋巴细胞增殖水平以及ＮＫ细胞活性显著增加，但Ｌｙｔ─２＋亚群（Ｔｓ）百分比不变。对环磷酰胺所诱发的免疫低反应，牡蛎提取物有回复和缓解作用，使已降低的总Ｔ、Ｔｈ、Ｔｈ／Ｔｓ，以及淋巴细胞增殖完全回复到正常对照水平，ＮＫ活性虽未达正常值，但也有明显回升（Ｐ＜０．０１）。表明牡蛎提取液有正向免疫调节功能。     

柳茶提取物免疫调节作用的实验研究

对服用柳茶提取物２ｗｋ的小鼠作了免疫机能和形态学方面的实验研究。结果表明：①柳茶的二种提取物均可显著促进淋巴细胞转化；增加正常小鼠抗绵羊红细胞抗体水平；改善腹腔巨噬细胞吞噬功能；水提取物尚能促进ＩＬ－２的产生。②对胸腺重量无影响，但明显增加脾重；光、电镜下见胸腺、脾脏内大量淋巴细胞增生、细胞代谢活跃等改变。提示：柳茶可能是一对免疫功能具多种作用的调节剂。     

紫外线减毒弓形虫对小鼠旋毛虫感染的影响

目的探讨紫外线减毒弓形虫免疫对小鼠旋毛虫感染的影响。方法ICR小鼠分为两组，实验组为紫外线减毒弓形虫免疫3周后再感染旋毛虫，对照组为旋毛虫单独感染。结果与旋毛虫单感染相比，小鼠预先经紫外线减毒弓形虫免疫再感染旋毛虫，在感染后5～14d其小肠内的成虫数明显增加（肠道排虫明显延迟），而感染后23-90d其肌肉中的幼虫数明显下降。结论紫外线减毒弓形虫免疫对小鼠旋毛虫感染具有一定的免疫调节和异源性保护作用。     

减毒增效升白汤对恶性肿瘤患者血液流变性及血小板的影响

恶性肿瘤患者血小板聚集、黏附功能亢进与肿瘤从发病到转移呈正相关。高纤维蛋白原血症．可加剧肿瘤血瘀证。益气活血中药可以改善病灶周围的微循环，减少肿瘤中的乏氧细胞。提高放疗敏感性，有利于化疗药物的渗入，从而提高治疗效果．现报道如下。     

醋酸舍莫瑞林拮抗环磷酰胺免疫抑制作用的实验研究

醋酸舍莫瑞林 (sermorelinacetate, SA)是人工合成的由29个氨基酸组成的生长激素释放素, 为内源性促生长激素释放激素(GHRH)的氨基末端片段, 具有显著的调节生长的效应 [1, 2], 其相对分子质量 (Mr)为 3 358. 03。Blacklock等 [3]提出, 神经肽 /神经递质、激素及细胞因子是神经系统、内分泌系统及免疫系统三大系统间相互调节的共用介质。免疫系统除本身非常精细的调节机制外, 还受到神经 内分泌 免疫网络的调节。我们观察了SA对环磷酰胺 (Cyclophosphamide,CY)所致免疫抑制作用的影响, 探讨了SA对机体细胞免疫功能的调节作用。1…     

硫普罗宁在晚期胃癌化疗中增效减毒作用的临床观察

胃癌是最常见的消化道恶性肿瘤,多数患者就诊时已属中、晚期,失去了最佳手术时机.对于不能手术切除的中晚期胃癌患者,化疗是提高疗效的主要措施,甚至为部分患者创造手术机会.FolFox(L-OHP CF/5-Fu)方案,是近年用于晚期胃癌治疗的一个疗效好、较成熟的方案,但其仍有较高的肝、肾毒性及骨髓抑制.因而预防和减轻化疗药物的不良反应成为目前研究的热点.     

家蝇蛹血淋巴及其提取物的免疫调节作用

目的:观察家蝇蛹血淋巴及其提取物对小鼠脾淋巴细胞增殖的影响.方法:以不同浓度血淋巴及其提取物与脾淋巴细胞、T细胞和B细胞共孵育72小时,采用MTT法测定淋巴细胞的吸光度值,观察它们对淋巴细胞增殖的促进作用,采用免疫印迹法研究提取物对B淋巴细胞增殖的信号转导通路.结果:与对照组相比,血淋巴冻干粉、分子量在50 kD以上的冻干粉及其提取物对混合淋巴细胞和B细胞增殖有显著促进作用,然而对于T细胞的增殖却没有明显的促进作用.MTT实验和免疫印迹结果表明血淋巴提取物激活了B淋巴细胞的ERK通路,促进了B淋巴细胞的增殖.结论:家蝇蛹血淋巴及其提取物具有免疫调节作用,为天然免疫增强剂的开发提供了一定的参考依据.     

白扁豆多糖对免疫抑制小鼠的免疫调节作用

目的探讨白扁豆多糖(polysaccharide from Dolichos lablab L.,DLP)对环磷酰胺(cyclophosphamide,CTX)所致的免疫抑制小鼠的免疫调节作用。方法小鼠随机分为正常对照组、模型组、香菇多糖(Lentinan,LNT,15 mg/kg)和白扁豆多糖低、中、高剂量组(75、150、300 mg/kg)。通过对小鼠连续3 d腹腔注射环磷酰胺(100 mg/kg)建立小鼠免疫抑制模型,造模后连续灌胃给药7 d,检测免疫器官重量指数、血清溶血素、脾淋巴细胞增殖、脾脏NK细胞活性及小鼠血清细胞因子IL-2、IL-4和INF-γ水平,观察白扁豆多糖的免疫调节作用。结果与正常对照组相比,模型组小鼠的免疫器官重量指数、血清溶血素、脾淋巴细胞增殖、脾脏NK细胞活性及小鼠血清细胞因子IL-2、IL-4和INF-γ水平均明显降低(P<0.05,P<0.01),而中、高剂量DLP和香菇多糖可明显减轻由环磷酰胺引起的上述各项指标的下降(P<0.05,P<0.01)。结论 DLP能改善环磷酰胺所致免疫抑制小鼠的免疫功能。     

环磷酰胺和嗜水气单胞菌对暗纹东方免疫抑制的研究

对暗纹东方分别注射 8、 0 8、 0 0 8mg/kg·bw的环磷酰胺 ,5d一次 ,连续 3次 ,并与一次性注射嗜水气单胞菌 (1× 1 0 5CFU/kg·bw )相比较 ,研究其对暗纹东方免疫功能的影响。结果显示 ,注射适当浓度的环磷酰胺和嗜水气单胞菌可明显减弱暗纹东方肝胰脏溶菌酶活性、脾脏NK细胞杀伤率、脾脏B淋巴细胞转化能力 ,显著降低白细胞吞噬指数和血清干扰素 (IFN α )含量 (P <0 0 5 )。选择 8mg/kg·bw环磷酰胺和 1× 1 0 5CFU/kg·bw的嗜水气单胞菌作为注射浓度可以抑制暗纹东方的免疫功能。相比之下 ,在试验范围内 ,环磷酰胺对暗纹东方免疫能力的抑制程度更大 ,范围更广 ,稳定性更好。     

Experimental Study of Ultralow-Dose Antibodies to Cyclophosphamide on Cyclophosphamide Myelotoxicity

The possibility of using ultralow-dose cyclophosphamide for reducing the myelotoxicity of cyclophosphamide, injected in the maximum permissible dose, was studied in mice. Combined treatment by the cytostatic and its ultralow-dose preparation led to a lesser suppression of the erythroid, lymphocytic, and particularly granulocytic hemopoiesis stems. This effect is explained by stimulation of the secretory activity of hemopoiesisinducing microenvironment and hence, of the functional activity of granulocytopoiesis under the effect of ultralow-dose cyclophosphamide. Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 147, No. 3, pp. 295–299, March, 2009     

The Effects of Cyclophosphamide on Antibody Dependent Cell-Mediated Cytotoxicity in Mice

Abstract

The effect of cyclophosphamide (CY) on antibody dependent cell-mediated cytotoxicity (ADCC) was evaluated. The results indicated that a single injection of CY markedly increased ADCC activity of murine splenic cells. This effect was dose dependent and was maximal on day 7 after the drug injection. The number of lymphoid cells in treated mice decreased to approximatedly 50%; however the percentages of EA rosettes were similar to those of control animals suggesting that the augmented cytotoxic activity was not due to a relative increase in Fc receptor bearing cells. CY treatment also enhanced delayed type hypersensitivity, but suppressed antibody production to sheep red blood cells. The possibility that CY eliminates a suppressor cell subpopulation that normally regulates ADCC levels is discussed.     

The Effects of Cyclophosphamide on Antibody Dependent Cell-Mediated Cytotoxicity in Mice

The effect of cyclophosphamide (CY) on antibody dependent cell-mediated cytotoxicity (ADCC) was evaluated. The results indicated that a single injection of CY markedly increased ADCC activity of murine splenic cells. This effect was dose dependent and was maximal on day 7 after the drug injection. The number of lymphoid cells in treated mice decreased to approximatedly 50%; however the percentages of EA rosettes were similar to those of control animals suggesting that the augmented cytotoxic activity was not due to a relative increase in Fc receptor bearing cells. CY treatment also enhanced delayed type hypersensitivity, but suppressed antibody production to sheep red blood cells. The possibility that CY eliminates a suppressor cell subpopulation that normally regulates ADCC levels is discussed.     

The Effects of Cyclophosphamide on Mitogen-Induced and Antibody-Dependent Cellular Cytotoxicity in Guinea Pigs

Lymph node cells from normal guinea pigs, when stimulated with the non-specific mitogen PHA were transformed to activated killer cells, capable of lysing ⁵¹Cr labeled mouse fibroblasts. Similarly, these lymphoid cells effected lysis of antibody coated chicken red cells in an antibody-dependent cellular cytotoxicity assay. Following cyclophosphamide, 150 mg/kg IP, the reactivity of an aliquot of lymph node cells to effect either cytotoxic reaction was not diminished. These results indicate that this immunosuppressant does not promote a selective decrease in either lymphoid effector. Rather, they are diminished in parallel with the generalized lympholysis resulting from drug administration. During the recovery phase, lymph node cells showed increased ability to lyse target cells, suggesting a rebound phase of heightened activity. Thymic cells from normal and cyclophosphamide treated animals were poor effectors in either cytotoxic assay. The addition of an equal number of thymocytes to lymph node cells resulted in decreased mitogen-induced cytotoxicity. Thymic inhibitory activity was mediated only by viable cells and the phenomenon did not represent an altered shift in PHA sensitivity. This suppressive activity persisted when thymic cells from cyclophosphamide treated-animals were employed, indicating that inhibitory cells were also not selectively depleted by this drug. In antibody-dependent cellular cytotoxicity assays, thymocytes from normal or cyclophosphamide-treated animals did not alter the cytotoxicity capacity of lymph node cells.     

Effects of Cyclophosphamide on Hemic Precursor Cells in Mouse Bone Marrow and Spleen

Cyclophosphamide severely inhibits the function of various hemic precursor cells in mice. In these studies we compared the effects of Cy on early B-lymphocytic precursor cells in mouse bone marrow to those effects on bone marrow myeloid precursor cells and splenic lymphoid precursor cells. These studies demonstrated that: 1) Pre-ARC in the bone marrow were extremely sensitive to even low doses of Cy (50 mg/kg) with virtually no renewal of this precursor population 11 days after injection of 200 mg/kg. 2) The sensitivity of pre-ARC to Cy along with the lack of their renewal was exemplified by the virtual absence of functional ARC in the spleen when assessed 11 days after injection of 200 mg/kg of Cy. 3) A rapid multiphasic renewal pattern was observed for myelocytic progenitor cells. 4) In general, LPS responsive cells were suppressed to a greater extent than were Con A responsive cells, especially with lower doses of Cy.     

The Effects of Cyclophosphamide on Mitogen-Induced and Antibody-Dependent Cellular Cytotoxicity in Guinea Pigs

Abstract

Lymph node cells from normal guinea pigs, when stimulated with the non-specific mitogen PHA were transformed to activated killer cells, capable of lysing ⁵¹Cr labeled mouse fibroblasts. Similarly, these lymphoid cells effected lysis of antibody coated chicken red cells in an antibody-dependent cellular cytotoxicity assay. Following cyclophosphamide, 150 mg/kg IP, the reactivity of an aliquot of lymph node cells to effect either cytotoxic reaction was not diminished. These results indicate that this immunosuppressant does not promote a selective decrease in either lymphoid effector. Rather, they are diminished in parallel with the generalized lympholysis resulting from drug administration. During the recovery phase, lymph node cells showed increased ability to lyse target cells, suggesting a rebound phase of heightened activity. Thymic cells from normal and cyclophosphamide treated animals were poor effectors in either cytotoxic assay. The addition of an equal number of thymocytes to lymph node cells resulted in decreased mitogen-induced cytotoxicity. Thymic inhibitory activity was mediated only by viable cells and the phenomenon did not represent an altered shift in PHA sensitivity. This suppressive activity persisted when thymic cells from cyclophosphamide treated-animals were employed, indicating that inhibitory cells were also not selectively depleted by this drug. In antibody-dependent cellular cytotoxicity assays, thymocytes from normal or cyclophosphamide-treated animals did not alter the cytotoxicity capacity of lymph node cells.     

Comparative Effects of Azathioprine, Cyclophosphamide and Frentizole on Humoral Immunity in Mice

Data is presented comparing the activities of three immunosuppressive agents, cyclophosphamide, frentizole and azathioprine in models of humoral immunity in mice. Cyclophosphamide and frentizole suppressed the primary and secondary plaque forming cell responses to sheep erythrocytes at lower doses than did azathioprine. Prolonged suppression of serum antibody titers occurred following short-term therapy with cyclophosphamide or frentizole, but not azathioprine. Azathioprine was also the least effective agent in suppressing a primary response to the T-independent antigen, trinitrophenylated lipopolysaccharide. All three agents were found to inhibit the induction and activity of suppressor cells at immunosuppressive doses.     

Comparative Effects of Azathioprine, Cyclophosphamide and Frentizole on Cellular Immunity in Mice

This report extends previous observations on the immunosuppressive properties of cyclophosphamide (CPA), azathioprine and frentizole (15) to include murine models of cellular immunity. Systemic and local graft vs host reactions (GVHR) were most effectively suppressed by CPA. In contrast to frentizole, both CPA and azathioprine were found to inhibit the proliferation of parental T-cells in a systemic GVHR. However, CPA was the only agent capable of inhibiting the proliferation of T-cells following contact sensitization with oxazolone.

Mice pretreated with a high dose of CPA or frentizole prior to inoculation with the murine sarcoma virus exhibited accelerated tumor growth. However, there was no accelerated growth of murine sarcoma virus induced tumors or an Sal spindle cell fibro-sarcoma during rather prolonged therapy with immunosuppressive doses of CPA, azathioprine or frentizole.

Normal mice treated with CPA showed a more drastic reduction in lymphoid elements of the spleen and thymus than mice treated with azathioprine or frentizole. Studies on the mitogenic responsiveness of spleen cells obtained from normal mice after an eight day course of therapy suggested that CPA has some selectivity of action on B-cells and azathioprine on T-cells.     

Acquired resistance to ticks. II. Effects of Cyclophosphamide on resistance.

Guinea-pig developed resistance to Dermacentor andersoni larvae after one infestation. Cyclophosphamide administered in one dose (300 mg/kg) 48 hr prior to an initial infestation with larvae blocked the acquisition of resistance. When cyclophosphamide was given in a similar regimen to guinea-pigs which had already acquired resistance, the expressin of resistance was partially blocked. It was proposed that the blockage of the acquisition of resistance further confirmed the immunological nature of tick resistance. Partial blockage of the expression of resistance by cyclophosphamide substantiated the presence of a humoral component to the resistance mechanism. The presence of a cell-mediated component was previously well established.