芦荟提取物C对小鼠移植性肿瘤及免疫功能的影响

目的：研究芦荟提取物C（Aloe Extract C，AE－C）对小鼠移植性肿瘤（实体瘤）的抑制作用和其对脾细胞IL－2分泌活性及NK细胞杀伤活性的影响。方法：建立AE－C的提取和主要成分含量测定法。用S180和MethA移植瘤动物模型为研究对象，经腹腔注射AE－C后，观察肿瘤组织的病理学改变并检测其脾细胞IL－2分泌活性和NK细胞杀伤活性。结果：AE－C能促使肿瘤组织大面积出血坏死及炎细胞浸润，按瘤组织坏死和炎细胞胞浸润分级积分法记录，AE－C治疗组明显高于对照组和5－FU治疗组（P＜0．01）。脾细胞IL－2分泌活性S180移植瘤AE－C治疗组与其对照组比较升高42．6％，MethA移植瘤AE－C治疗组与其对照组比较升高62．6％。NK细胞杀伤尖性AE－C治疗组较对照组有明显的升高（P＜0．01）。5－FU治疗组小鼠免疫功能明显受到抑制。结论：AE－C有抑制肿瘤和调节机体免疫功能的作用。     

自然杀伤细胞对小鼠HepS肝癌移植瘤的抑制作用研究

目的 研究自然杀伤(NK)细胞对原发性肝癌Heps移植瘤小鼠的治疗作用和机理。方法 建立小鼠移植性肝癌(Heps)实体瘤模型,随机分为生理盐水(NS)组、治疗1组(输注的NK细胞数为1×10⁴/只)、治疗2组(输注的NK细胞数为1×10⁵/只)和治疗3组(输注的NK细胞数为1×10⁶/只),每组15只。接种肝癌细胞当天,分别于尾静脉注射不同数量的NK细胞,对照组注射NS。观测小鼠移植瘤体积及各组小鼠平均生存时间。各组于输注NK细胞后第15天分别处死2只小鼠,对移植瘤组织切片进行HE染色,用流式细胞术(FCM)检测脾细胞NK的含量;乳酸脱氢酶(LDH)释放法检测脾细胞杀伤活性。结果 接种移植瘤后第8天,治疗3组移植瘤的生长速度较其他组小鼠显著减慢(P＜0.05)。第20天时治疗1组移植瘤体积明显小于对照组(P＜0.05),治疗2组和3组移植瘤体积非常显著小于对照组(P＜0.01)。治疗1组小鼠平均生存期明显长于对照组和治疗2、3组(P＜0.01)。治疗1-3组脾细胞杀伤活性以及NK细胞的含量高于对照组(P＜0.01)。结论 适量输注NK细胞可以有效抑制HepS肝癌移植瘤的生长,延长小鼠的生存期,为临床应用NK细胞治疗时数量的选择提供了实验依据。     

硒酸酯多糖增强荷瘤小鼠免疫功能和自身肿瘤杀伤活性的作用

本文研究了硒酸酯多糖(KSC)对荷S180肉瘤小鼠NK细胞活性、LAK细胞活性、IL-2分泌能力和自身肿瘤杀伤活性(ATK)的影响及抑癌效应.结果表明,KSC(40mg/kg·d×9d,ig)能增强荷瘤鼠NK细胞和LAK细胞活性,促进脾细胞产生IL-2,增强ATK活性;加强环磷酰胺(Cy,20mg/kg·d×9d,ip)的抑瘤作用,并能拮抗Cy对免疫活性细胞的抑制效应.体外用rIL-2激活荷瘤鼠脾淋巴细胞可诱生或增强ATK活性.本研究结果提示,KSC上调肿瘤宿主NK细胞和LAK细胞活性及IL-2的分泌水平,增强ATK活性,可作为生物反应调节剂(BRM)应用于肿瘤生物治疗.     

肿瘤患者自然杀伤细胞活性水平及其临床意义

目的　研究恶性肿瘤患者外周血自然杀伤 (NK)细胞活性及其临床意义。方法　采用LDH释放法对 43名健康成年人及 2 6 7例肿瘤患者进行了外周血NK细胞活性测定。结果　恶性肿瘤患者NK细胞活性显著低于正常对照组 (P <0 .0 0 1)。伴转移患者NK细胞活性降低更明显 ,与不伴转移者相比 ,差异显著 (P <0 .0 0 0 5 )。化疗及放疗后NK细胞活性显著降低 (P <0 .0 1) ,而IL 2治疗后NK细胞活性显著升高 (P <0 .0 1) ,但低于正常对照组 (P <0 .0 1)。结论　NK细胞活性显著降低与恶性肿瘤发生、发展及转移相关 ,监测NK细胞活性有助于评价肿瘤患者治疗过程中的免疫功能。     

NK细胞对人鼻咽癌细胞CNE2裸鼠皮下移植瘤的抑制作用

 目的 研究同种异体NK细胞对人鼻咽癌细胞（CNE2）裸鼠皮下移植瘤的抑制作用。方法PCR-SSP法检测CNE2细胞HLA-A、B、Cw表型、NK细胞KIR表型（选择3例健康者为试验对象）,磁珠分离法分离NK细胞并进行体外培养扩增,LDH释放法测定NK细胞对CNE2细胞的体外杀伤活性。12只BALB/c裸鼠分为两组,每组6只,对照组裸鼠每只皮下接种1×106CNE2细胞,治疗组裸鼠每只皮下接种1×106CNE2细胞,同时每只经尾静脉注入3×107NK细胞,观察两组裸鼠成瘤时间、成瘤率、肿瘤体积变化、计算抑瘤率。结果 CNE2细胞表面HLA-A、B、Cw表型为A2,24;B18,35;Cw4,7,3例健康者均表达KIR2DL1、KIR2DL3、KIR3DL1、KIR3DL2。效靶比5∶1、10∶1、20∶1、30∶1时,NK细胞对CNE2细胞的杀伤活性分别为（9.37±2.14）%、（27.14±1.82）%、（36.40±4.28）%and（54.67±2.80）%。对照组和NK细胞治疗组肿瘤出现时间分别为（10.00±2.68）d、（18.80±1.64）d,（P〈0.01）,成瘤率分别为100%（6/6）、83.33%（5/6）,对照组和NK细胞治疗组裸鼠的瘤重分别为（2.22±0.09）g、（1.42±0.09）g,（P〈0.01）,NK治疗组的抑瘤率为36.04%。肿瘤组织石蜡切片病理学鉴定为低分化鳞状上皮细胞癌,NK细胞治疗组可见角化肿瘤细胞,较多的淋巴细胞浸润和大量细胞坏死区。结论 NK细胞对鼻咽癌裸鼠皮下移植瘤有明显的抑制作用,有希望成为治疗鼻咽癌的新方法。     

芦荟提取物C诱生小鼠肿瘤坏死因子的研究

目的 :研究芦荟提取物C(aloeextractC ,AE C)在BALB C鼠体内诱导产生肿瘤坏死因子 (tu mornecrosisfactor ,TNF)。方法 :连续 5d给小鼠注射AE C ,第 6天取血分离血清 ,应用结晶紫染色法测其TNF活性 ,观察经AE C诱生的鼠血清对多种瘤细胞的杀伤作用 ,杀伤作用的持续时间和对温度的敏感性及血清不同稀释度的杀伤效果。结果 :AE C能诱导小鼠产生TNF α ,与对照组比较作用明显 (P <0 0 1) ;并且对多种靶细胞有显著的杀伤作用 ;TNF活性 2 4h达高峰 ,第 4天下降明显 ,5d接近正常水平 ;血清标本稀释至 2 0 0倍时 ,仍具有较强的杀伤活性 ;诱生后的TNF有一定的温度敏感性。结论 :芦荟提取物C有诱生BALB C鼠产生肿瘤坏死因子的作用     

联合过继免疫细胞输注小鼠后DC、NK分布的研究

目的：观察自然杀伤（NK）细胞／树突状细胞（DC）联合过继免疫治疗小鼠皮下黑色素瘤时效应细胞在荷瘤小鼠体内的分布。方法：建立C57BL/6小鼠皮下黑色素瘤模型。体外培养增殖小鼠NK细胞、DC并标记，以不同比例混合两种细胞，分别以静脉注射和瘤内注射的方式回输荷瘤小鼠体内．于注射后不同时间点取肿瘤、肝、脾、肺组织进行切片，观察各组织中效应细胞的数量及分布。结果：静脉注射组NK细胞、DC主要分布在肿瘤微循环及实质组织中，各时间点NK细胞、DC的浸润数量有显著差异（P〈0．01），注射后4h浸润的效应细胞最多．12h最少，在脾脏中见少量NK细胞的分布，在肝脏及肺组织中偶见。瘤内注射组NK细胞、DC主要分布在肿瘤实质组织中，各观察时间点NK细胞、DC的浸润数量有显著差异（P〈0，01）．注射后1h浸润的效应细胞最多，12h最少，在肝、脾、肺组织中未见NK细胞、DC分布。两种注射方式下按不同比例混合进行NK细胞、DC的过继治疗，各组间差异具有显著性（P〈0.01），混合注射组效应细胞在肿瘤组织内的浸润多于单独注射组。结论：NK细胞、DC免疫过继后能够“靶向性”聚集在肿瘤周围及肿瘤内部，对肿瘤具有治疗作用．NK细胞、DC联合过继免疫治疗效果优于单独注射，提示NK细胞、DC联合输注可能成为肿瘤生物治疗的新模式。     

脐血CD_3AK细胞的制备、生物活性测定及临床应用初探

 目的　研究用脐血单个核细胞制备CD3 AK细胞的抗肿瘤作用 ,探讨肿瘤生物治疗近期疗效的免疫指标。方法　分离脐血单个核细胞 ,分别用IL 2和IL 2 +CD3 Ab诱导LAK和CD3AK细胞 ,并测其扩增数量和对K5 6 2细胞的杀伤活性 ;测定肿瘤患者用CD3 AK细胞治疗前后外周血单核细胞(PBMC)的NK杀伤活性。结果　脐血LAK细胞和脐血CD3 AK细胞均于培养后第 11天时扩增倍数最高 ,分别是培养前的 18倍、2 4倍 ,对K5 6 2的杀伤活性分别是培养前的 2 .6倍和 3.2倍 ;肿瘤患者输注CD3 AK细胞一疗程后 ,其PBMC的NK杀伤活性由 6 2 %升高到 82 % ,平均升高 32 %。结论　 (1)脐血单个核细胞是LAK细胞和CD3 AK细胞良好的前体细胞。 (2 )LAK和CD3 AK细胞的数量和杀伤能力在培养的第 11天时达高峰 ,而且CD3 AK细胞数量和杀伤活性明显优于LAK细胞。 (3)CD3 AK细胞输注能明显提高肿瘤患者PBMC的NK活性。 (4 )肿瘤病人PBMC的NK活性测定可望成为肿瘤生物治疗的一个近期疗效参数     

表达白细胞介素-12质粒DNA抗小鼠肝癌皮下移植瘤的作用

目的 探讨瘤内注射mIL-12质粒DNA抗小鼠肝癌皮下移植瘤的作用。方法：构建真核表达质粒载体pDC511mIL-12，ELISA方法检测质粒载体在真核细胞中的表达，淋巴母细胞增殖法检测mIL-12的生物学活性；分别于小鼠肝癌H22皮下移植瘤内直接注射质粒DNA，观察各组小鼠存活时间、肿瘤体积变化及各组小鼠脾脏细胞毒T淋巴细胞(CTL)的活性：注射质粒DNA后1月进行瘤体组织病理学观察：结果：mIL-12基因治疗组与空载体对照组相比，肿瘤生长显著受抑制(F=4．10，P=0．03)，小鼠存活期显著延长(X^2=4．48，P=0．03)．并且小鼠脾细胞CTL杀伤活性增强。质粒DNA瘤内注射1月后，pDC511mIL-12组肿瘤病灶炎性细胞浸润明显，病灶内肿瘤细胞广泛坏死。结论：瘤内注射mIL-12表达质粒DNA可抑制小鼠肝癌皮下移植瘤生长，能提高机体抗肿瘤免疫应答。     

自体肿瘤瘤苗对荷瘤鼠Th1、Th2型细胞因子及细胞毒作用的影响

目的研究经处理的H22肝癌细胞肿瘤瘤苗作为全细胞瘤苗对H22荷瘤小鼠体内Th1/Th2细胞比例和细胞因子的影响以及CTL的杀伤活性.方法用加重组白细胞介素2、重组粒细胞单核细胞集落刺激因子及福氏不完全佐剂制成疫苗,建立荷瘤小鼠模型,用51Cr释放法测定瘤苗免疫组、荷瘤组、正常组小鼠脾细胞对亲本H22肝癌细胞的杀伤活性;流式细胞仪检测单个核细胞中的Th1和Th2细胞,并取血检测血清中IL-10、IFN-γ水平.结果效靶比为200:1时,免疫小鼠脾细胞体外杀伤亲本H22肝癌细胞的杀伤率为38.3%,显著高于荷瘤组的13.6%,正常组的7.5%,以及对S180细胞的9.1%(P均＜0.05).瘤苗免疫组Th1细胞及Th1/Th2细胞的比值显著升高(P＜0.01),血清IFN-γ较对照组明显升高(P＜0.01);血清IL-10较对照组明显降低(P＜0.01).结论肿瘤细胞加小剂量IL-2和GM-CSF及佐剂组成的肿瘤细胞瘤苗可激发特异性细胞介导的免疫反应,改善抗肿瘤免疫反应.     

Anti-tumor Effects of Interleukin-4 and Interleukin-5 against Mouse B Cell Lymphoma and Possible Mechanisms of Their Action

We investigated the anti-tumor effects of recombinant mouse interleukin (IL)-4 and IL-5 by using a transplantable B cell lymphoma 38C13 cell line as a model. Daily local administration of either IL-4 or IL-5 produced moderate but significant inhibition of the rate of local tumor growth and prolongation of mean survival time (MST) in syngeneic C3H/HeJ mice; these anti-tumor effects appeared to plateau at low doses. Histopathologic and immuno-histochemical examination revealed necrotic changes in the cytokine-treated tumors, associated with infiltration of inflammatory cells such as eosinophils, macrophages, and lymphocytes. The infiltrating lymphocytes were found to be Thy-1.2⁺ T cells. To elucidate the importance of T cells, the rate of tumor growth and the MSTs were compared between athymic T cell-deficient BALB/c nude mice and immunocompetent C3H/HeJ mice. In the nude mice the transplanted tumor grew more rapidly and the MST was shorter than in the normal mice, suggesting a significant contribution of infiltrating T cells in the anti-tumor effects of the interleukins. Lastly, in vitro, growth inhibition of the 38C13 cells was observed in a dose-dependent manner at relatively high concentrations of either cytokine. Therefore, we conclude that both IL-4 and IL-5 have moderate anti-tumor effects against 38C13 B cell lymphoma both in vivo and in vitro , and that the observed in vivo anti-tumor effects are probably mediated both by tumoristatic action of infiltrating cells, such as eosinophils, macrophages and T lymphocytes, and by direct anti-proliferative action of the recombinant cytokines.     

Augmentation by Tumor Necrosis Factor α of the Systemic Therapeutic Effect of Lymphokine-activated Killer Cells in Adoptive Immunotherapy of Murine Tumor

The therapeutic effect of a combined modality of lymphokine-activated killer (LAK) cells and tumor necrosis factor α (TNFα) on MBL-2 tumor in C57BL/6 mice was studied. Murine LAK cells induced from splenocytes by interleukin 2 (IL2) could lyse MBL-2 target cells in vitro , but no enhancement of the LAK activity was found by the treatment of LAK cells with TNFα in vitro. However, the treatment of MBL-2 with TNFα enhanced the sensitivity to LAK cells. Moreover, administration of TNFα to mice bearing solid MBL-2 tumor led to increased tumor vascular permeability within 1 h, and resulted in the enhanced accumulation of systemically transferred LAK cells in tumor tissue. Based on these results, we treated MBL-2-bearing mice with TNFα and then with LAK cells 1 h later, No therapeutic effect was observed when tumor-bearing mice were treated with TNFα alone or LAK cells plus IL2. However, adoptive immunotherapy using LAK cells and TNFα had therapeutic effects, i.e. growth inhibition of tumor nodules and prolongation of survival. These results indicated that appropriately timed pretreatment of tumor-bearing mice with TNFα augmented the anti-tumor efficacy of LAK cells.     

苦参碱对荷瘤小鼠抑瘤作用的实验研究

目的观察苦参碱的体内抗肿瘤活性,初步探讨其体内抑瘤作用机制。方法采用小鼠H22肝癌细胞实体瘤模型进行体内抑瘤实验,观察荷瘤动物的生长情况和肿瘤生长曲线,测定肿瘤生长抑制率;肿瘤组织病理学切片进行HE染色形态学观察,其超微结构行透射电镜观察。结果苦参碱对小鼠的H22实体瘤生长具有明显的抑制作用,抑瘤率达60％以上。苦参碱处理组小鼠的成瘤时间明显晚于生理盐水对照组,肿瘤生长也较对照组慢。组织学观察显示,肿瘤细胞大量变性坏死,电镜下可见凋亡细胞和凋亡小体。结论苦参碱具有较强的体内抗肿瘤作用,作用机制可能与其能够抑制肿瘤细胞的分裂和增殖、直接杀伤肿瘤细胞和(或)诱导肿瘤细胞凋亡、调节机体的抗肿瘤免疫应答效应有关。     

Anti-tumor effects of interleukin-4 and interleukin-5 against mouse B cell lymphoma and possible mechanisms of their action.

We investigated the anti-tumor effects of recombinant mouse interleukin (IL)-4 and IL-5 by using a transplantable B cell lymphoma 38C13 cell line as a model. Daily local administration of either IL-4 or IL-5 produced moderate but significant inhibition of the rate of local tumor growth and prolongation of mean survival time (MST) in syngeneic C3H/HeJ mice; these anti-tumor effects appeared to plateau at low doses. Histopathologic and immuno-histochemical examination revealed necrotic changes in the cytokine-treated tumors, associated with infiltration of inflammatory cells such as eosinophils, macrophages, and lymphocytes. The infiltrating lymphocytes were found to be Thy-1.2+ T cells. To elucidate the importance of T cells, the rate of tumor growth and the MSTs were compared between athymic T cell-deficient BALB/c nude mice and immunocompetent C3H/HeJ mice. In the nude mice the transplanted tumor grew more rapidly and the MST was shorter than in the normal mice, suggesting a significant contribution of infiltrating T cells in the anti-tumor effects of the interleukins. Lastly, in vitro, growth inhibition of the 38C13 cells was observed in a dose-dependent manner at relatively high concentrations of either cytokine. Therefore, we conclude that both IL-4 and IL-5 have moderate anti-tumor effects against 38C13 B cell lymphoma both in vivo and in vitro, and that the observed in vivo anti-tumor effects are probably mediated both by tumoristatic action of infiltrating cells, such as eosinophils, macrophages and T lymphocytes, and by direct anti-proliferative action of the recombinant cytokines.     

树突状细胞与肿瘤细胞融合后诱导T细胞介导的抗肿瘤效应

目的：研究树突状细胞（DC）与肿瘤细胞（SP2／0）融合作为肿瘤疫苗免疫小鼠后抑制肿瘤生长的作用及其机理。方法：BALB／C小鼠DC与SP2／0细胞体外融合,形成的杂交瘤分2次免疫接种同基因小鼠皮下,然后用SP2／0细胞攻击免疫的小鼠,观察肿瘤的生长情况及免疫小鼠脾细胞特异性CTL功能。结果：DC－SP2／0杂交瘤接种小鼠能产生明显的抗肿瘤效应,其拮抗SP2／0细胞攻击的能力明显强于用灭活的死SP2／0细胞与DC混合,和单用死SP2／0细胞免疫的小鼠及用生理盐水的对照组小鼠。DC－SP2／0杂交瘤免疫接种小鼠的脾细胞特异性CTL杀伤活性强于其它各组小鼠。结论：DC与肿瘤细胞融合后作为肿瘤疫苗接种可在体内产生明显的抗肿瘤免疫,其机理主要是特异性CTL的作用。     

AK细胞及环磷酰胺治疗肝癌的实验研究

为研究１ 种新的过继免疫化疗治疗肝癌的方法,采用肝癌细胞株Ｈ２２ 接种于近交系Ｂａｌｂ／ｃ 小鼠皮下,制成肿瘤模型。使用ＩＬ２ 、肿瘤活化的杀伤细胞（ＡＫ细胞）及环磷酰胺（Ｃｙ） 进行治疗,检测小鼠脾淋巴细胞ＮＫ、ＬＡＫ及ＣＴＬ 活性,用流式细胞仪检测Ｌ３Ｔ４ 亚群及Ｌｙｔ２ 亚群含量。结果表明在过继免疫化疗组小鼠ＬＡＫ 及ＣＴＬ活性明显高于其它治疗组（Ｐ＜ ０．０１）,荷瘤小鼠肿瘤结节生长较ＩＬ２ 组及Ｃｙ 组明显缓慢（Ｐ＜ ０．０１）,生存期也明显高于其它各治疗组（Ｐ＜０ ．０１）。该研究表明过继免疫化疗有较强的抗肿瘤作用。     

Effect of cyclooxygenase and nitric oxide synthase inhibitors on tumor growth in mouse tumor models with and without cancer cachexia related to prostanoids

The potential interaction between cyclooxygenase (Cox) and NO metabolic pathways in the control of local tumor growth was evaluated. Mice bearing either a sarcoma-derived tumor (C57B1; MCG 101) or a malignant melanoma (C3H/HeN; K1735-M2) were used. These models were principally different because they demonstrate, in tumor hosts, conditions with and without cancer cachexia, seemingly related to high and low production of prostanoids, respectively. Cox inhibitors (Cox-1 and Cox-2) decreased tumor growth by 35-40% in MCG 101-bearing mice but had no such effect on melanoma-bearing mice, despite the expression of the Cox-2 protein in melanoma cells. Indomethacin reduced prostanoid production in both tumor (MCG 101) and host tissues and reduced tumor cell proliferation, mainly in vivo. Nitric oxide synthase (NOS) inhibitors (N(omega)-nitro-L-arginine methyl ester and N(omega)-nitro-L-arginine) reduced tumor growth in vivo by approximately 50% in both tumor models. Tumor growth reduction, related to NOS inhibition, was unrelated to prostanoid production and was an in vivo phenomenon in both tumor models. Specific inhibitors of inducible NOS activity, unexpectedly, had no effect in any tumor model, although inducible NOS protein was present in tumor tissues in large amounts. A combination of Cox and NOS inhibitors had no additive effect on tumor growth (MCG 101). Cox inhibition increased tumor tissue (MCG 101) expression of cNOS mRNA but had no significant effect on tumor tissue expression of the transferrin receptor, vascular endothelial growth factor, or basic fibroblast growth factor. NOS inhibition increased tumor tissue content of cNOS mRNA but showed as well a trend to increase mRNA content of the transferrin receptor and vascular endothelial growth factor. Our results suggest that NOS inhibitors can decrease the local growth of tumors that are either responsive or unresponsive to Cox inhibition. This effect may reflect cross-talk between Cox and NOS pathways within or among tumor cells, or it may represent unrelated effects on tumor and host cells. Whether NO inhibition may be used therapeutically in clinical tumors that are unresponsive to eicosanoid intervention remains to be evaluated.     

IL-24基因对大鼠胶质瘤细胞生长状况的影响

目的　探讨IL 2 4基因对C6大鼠胶质瘤细胞生长状况的影响。方法　应用逆转录病毒载体 ,将IL 2 4基因导入C6细胞 ,经G4 18筛选后获得表达IL 2 4分子的阳性细胞克隆C6 /IL 2 4 ;用RT PCR方法检测目的基因表达 ;四甲基偶氮唑蓝 (MTT)法检测细胞体外增殖状况 ,流式细胞技术检测细胞的增殖活性 ,并制作荷瘤动物模型 ,观察C6 /IL 2 4和C6细胞的体内致瘤性。结果　RT PCR检测表明 ,外源IL 2 4基因于mRNA水平在C6 /IL 2 4细胞已获得稳定表达。C6 /IL 2 4细胞系的体外增殖性较亲代C6细胞明显下降 ,流式细胞术检测其细胞增殖指数 (PI)为 (2 9.71± 0 .89) %。 9只接种C6 /IL 2 4细胞的实验组大鼠中 ,6只颅内成瘤 ,肿瘤体积为 (14 .0 8± 9.81)mm3 ,明显小于接种C6细胞大鼠的肿瘤体积 (P <0 .0 5 )。结论　外源性IL 2 4基因可部分抑制胶质瘤细胞异常增殖的肿瘤特性。     

中药合剂“振明正生”对三株人肿瘤细胞裸鼠移植瘤抑制作用的观察

目的：观察中药合剂＂振明正生＂（ZMZS）对人肿瘤细胞的抑制作用。方法：BALB/c裸鼠分别接种人白血病细胞系（K562）、鼻咽癌细胞系（CN1）和胰腺癌细胞系（P3）,2×106/只。接种后24小时开始给药,实验组裸鼠每天口服中药合剂0.2ml/只,连续4周。对照组裸鼠口服生理盐水0.2ml/只。每周测量动物肿瘤大小,计算肿瘤生长抑制率。结果：经过3或4周的治疗,中药合剂＂振明正生＂对K562、CN1和P3有明显抑制作用。结论：中药合剂＂振明正生＂对三株人肿瘤细胞裸鼠移植瘤有显著的治疗效果。