H4化合物抗肿瘤活性研究

目的研究化合物H4的体内外抗肿瘤活性。方法以人早幼粒白血病细胞株HL-60、人红细胞白血病细胞株K562、人肺癌细胞株A549、人卵巢癌细胞株HO-8910、人乳腺癌细胞株Bcap-37、人结肠癌细胞株Colo-320和人胃癌细胞株BGC-823为模型,采用改良MTT法检测H4对肿瘤细胞增殖的影响;以小鼠肉瘤S180和小鼠肝癌H22为移植性肿瘤模型,检测H4对小鼠肿瘤生长的抑制作用。结果化合物H4对多株肿瘤细胞增殖均显示了明显的抑制活性,IC50在0.042～3.651mg.L-1之间;对S180和H22的生长显示了一定的抑制作用,在900mg.kg-1时肿瘤生长抑制率分别为49.08%、41.33%。结论化合物H4具有较强的体内、外抗肿瘤活性。     

二硫键稳定的人源性抗bFGF双链抗体抑制人肺癌细胞生长的作用研究

目的研究二硫键稳定的人源性抗b FGF双链抗体(ds-Diabody)对人肺癌A549细胞的体内外增殖抑制作用。方法利用镍离子亲和层析和离子交换层析的方法纯化得到ds-Diabody,间接ELISA检测其抗原结合活性,CCK-8法检测ds-Diabody对人肺癌A549细胞的增殖抑制作用,Western blot分析其作用于肿瘤细胞的机制,Transwell检测其对肿瘤细胞迁移侵袭的影响。建立裸鼠皮下移植瘤模型,记录各处理组裸鼠皮下移植瘤的体积及裸鼠体质量变化。免疫组化法检测肿瘤组织CD31和LYVE1的表达情况,初步探讨抗b FGF的人源性ds-Diabody抗体的抗肿瘤机制。结果成功纯化得到具有抗原结合活性的ds-Diabody。CCK-8结果显示,纯化的ds-Diabody可剂量依赖性地抑制人肺癌A549细胞株的增殖。Western blot结果表明ds-Diabody能有效阻断与b FGF相关的MAPK和Akt通路。Transwell结果表明ds-Diabody可以显著抑制A549细胞的迁移及侵袭。裸鼠体内试验中,ds-Diabody抗体显著地抑制了肿瘤的生长,抑制率为86.54%。免疫组化的结果显示ds-Diabody抗体处理组肿瘤组织中微血管密度和淋巴管密度均有下降。结论抗bFGF的人源性ds-Diabody抗体可有效地抑制人肺癌A549细胞的生长。     

放射诱导正反馈基因环路调控Wt-p53表达对肺腺癌移植瘤的抑制作用

目的:探讨放射控导的wt-p53蛋白正反馈基因环路对肺腺癌细胞裸鼠移植瘤放射增敏作用及机制。方法:将治疗组pE6R4-p53-EGFP/H1299细胞和对照组pE6-p53-EGFP/H1299、pR4-p53-EGFP/H1299、H1299(p53-/-)细胞分别注射于裸鼠背部皮下,建立裸鼠移植瘤模型;X线照射后,绘制肿瘤生长曲线;计算各组抑瘤率;免疫组化法检测瘤组织wt-p53表达;计算TCD50及放射增敏比(SER)。结果:pE6R4-p53-EGFP/H1299+IR组移植瘤生长明显受抑制,抑瘤率(86.41%)明显高于对照组pE6-p53-EGFP/H1299+IR组(70.76%)、pR4-p53-EGFP/H1299+IR组(35.53%)和H1299+IR组(12.58%)。免疫组化提示pE6R4-p53-EGFP/H1299组比pR4-p53-EGFP/H1299、pE6-p53-EGFP/H1299组wt-p53蛋白表达量明显增高。pE6R4-p53-EGFP/H1299组和对照组pE6-p53-EGFP/H1299和H1299(p53-/-)荷瘤鼠TCD50分别为12.1Gy、15.2Gy和19.4Gy,SER分别为1.6和1.28。结论:放射控导的wt-p53蛋白正反馈基因环路能在体内正常激活并发挥抗肿瘤生物学效应,且显著增加了瘤组织对放射的敏感性。     

重组人源化抗人HGF单克隆抗体鉴定及其抗肿瘤活性研究

目的对人源化抗肝细胞生长因子(hepatocyte growth factor,HGF)单克隆抗体进行初步鉴定,并对其体内、外抗肿瘤活性及药代动力学特征进行研究。方法将基因工程技术制备的2株抗HGF人源化单克隆抗体HE19-12和HD19-27,通过UV、SDS-PAGE方法对其质量浓度、相对分子质量及纯度进行鉴定;MTT法评价抗体对人脑胶质瘤U87MG细胞的增殖抑制活性,并比较抗体人源化前后活性差异;采用ELISA法评价抗体结合HGF及竞争抑制HGF与受体结合的能力;Transwell法研究抗体对HGF促进PC-3细胞迁移的抑制能力;通过构建U87MG裸鼠移植瘤模型,比较抗体在体内的抗肿瘤作用;抗体通过静脉给予正常小鼠,分析其药代动力学特征。结果 2株抗体单体纯度均达到90%以上,均可抑制U87MG肿瘤细胞增殖,且人源化前后抗体活性差异不大。2株抗体均与HGF具有较强的结合能力,且可竞争抑制HGF与其受体C-Met的结合。细胞迁移实验显示,2株抗体具有抑制HGF促肿瘤细胞迁移的能力。裸鼠移植瘤试验显示HGF抗体可有效抑制肿瘤的生长,其中HE19-12在试验中显示更好的抗肿瘤活性。小鼠药代结果显示,HE19-12和HD19-27的半衰期分别为423.3 h和342.5 h。结论成功对制备出的2株人源化单克隆抗体进行初步鉴定及一系列抗肿瘤活性研究,证明具有较强抗肿瘤活性的HGF中和抗体,且具有良好的药代动力学特征,为HGF/C-Met靶点抗肿瘤药物的开发奠定基础。     

癌前状态和NK细胞

近年来,许多报告提示NK细胞对于恶性肿瘤的发生、增殖可能起重要作用.但NK细胞,特别是人NK细胞对肿瘤细胞的作用尚无定论;NK细胞在体内是否真的控制癌的发生和增殖仍不明确.近年,笔者曾对有白血病前兆患者的NK细胞进行了动态观察,获得了饶有兴趣的发现.本文拟介绍癌前状态及生癌时NK细胞在体内的作用,从而对人NK细胞的抗肿瘤作用加以探讨.NK细胞的抗肿瘤作用以往曾认为抗肿瘤增殖的免疫防御主要是T淋巴细胞,但越来越多的报告认为未必如此.在T淋巴细胞功能缺陷而保留有NK细胞活性的裸鼠,仍显示有对同系或同种的移植肿瘤的抵抗力.亚同系A、F_1杂交小鼠     

miR-520c-3p靶向MEX3A调控肺癌细胞增殖、凋亡的分子机制

为研究miR-520c-3p对肺癌细胞增殖和凋亡的影响及其潜在的作用机制,用实时定量RT-PCR检测肺癌细胞H1299、NCI-H460、A549和正常肺上皮细胞BEAS-2B中miR-520c-3p和MEX3同源物A(MEX3 homolog A,MEX3A)的表达水平。将miR-NC、miR-520c-3p、si-NC、si-MEX3A、anti-miR-NC、anti-miR-520c-3p转染至H1299细胞后,用细胞计数试剂盒8(cell counting kit 8,CCK-8)法检测细胞增殖,流式细胞术检测细胞凋亡,Western blotting检测蛋白表达,双荧光素酶报告基因检测实验检测细胞的荧光活性。结果显示,与正常肺上皮细胞BEAS-2B比较,肺癌细胞H1299、NCI-H460、A549中miR-520c-3p的表达水平均显著降低(P0.05),MEX3A mRNA和蛋白的表达水平显著升高(P0.05)。miR-520c-3p过表达、MEX3A抑制表达均可抑制H1299细胞的增殖活力,促进细胞凋亡;miR-520c-3p过表达抑制CyclinD1、Bcl-2蛋白的表达,促进p21、Cleaved Caspase-3、Bax蛋白的表达;MEX3A抑制表达抑制CyclinD1、Bcl-2蛋白的表达,促进p21、Bax蛋白的表达。miR-520c-3p可靶向调控MEX3A的表达;MEX3A过表达逆转了miR-520c-3p过表达对肺癌细胞H1299的增殖抑制和凋亡促进作用。提示miR-520c-3p可抑制肺癌细胞H1299的增殖,促进其凋亡,其机制可能与靶向MEX3A有关,这将为肺癌的预防和治疗提供新靶点。     

贝母素乙抑制结肠癌细胞生长及裸鼠成瘤

目的研究贝母素乙对结肠癌细胞生长以及裸鼠成瘤的影响.方法体外试验检测贝母素乙对结肠癌SW480细胞增殖和侵袭的影响,以及Ki67、PCNA、VEGF、E-cadherin、N-cadherin、HIF-1α、Akt/p-Akt表达水平;构建结肠癌移植瘤裸鼠模型,分析贝母素乙体内抗肿瘤活性及HIF-1α、VEGF、Akt/p-Akt表达影响.结果贝母素乙能够明显抑制SW480细胞克隆增殖和侵袭(P<0.05),降低Ki67、PCNA、N-cadherin、E-cadherin、HIF-1α、p-Akt/Akt表达量(P<0.05),升高Vimentin表达水平(P<0.05),还可以抑制肿瘤增长,抑制移植瘤组织Ki67、VEGF、HIF-1α、p-Akt/Akt表达(P<0.05).结论贝母素乙可能通过抑制Akt信号通路,抑制结肠癌SW480细胞克隆增殖、侵袭和裸鼠移植瘤的生长.     

下调TCF3抑制非小细胞肺癌细胞的增殖和迁移能力

目的:探索下调T细胞因子3(TCF3)抑制非小细胞肺癌细胞增殖和迁移的分子机制。方法:运用Lipofectamine 2000转染法将siTCF3和阴性对照siRNA(NCsiRNA)转染非小细胞肺癌A549和H1299细胞;运用real-time PCR和Western blot分别测定TCF3的mRNA和蛋白水平;运用萤光素酶报告基因实验测定TCF3的转录活性;MTT、克隆形成实验、Transwell实验和Annexin V-FITC/PI染色联合流式细胞术分别测定细胞的活力、克隆形成能力、转移能力及细胞凋亡率;Western blot检测Wnt、c-Myc、基质金属蛋白酶(MMP)-9、MMP-13、金属蛋白酶组织抑制物(TIMP)-1的蛋白表达水平。结果:与NCsiRNA转染组的细胞比较,siTCF3显著抑制A549细胞和H1299细胞中TCF3的mRNA和蛋白水平(P0.01)。TCF3转录活性和c-Myc蛋白表达水平明显低于NCsiRNA细胞(P0.05)。MTT实验结果显示,培养24 h、48 h、72 h和96 h的A549-siTCF3和H1299-siTCF3细胞活力均显著低于NCsiRNA细胞(P0.05)。与NCsiRNA细胞相比,siTCF3显著抑制A549细胞和H1299细胞的克隆形成能力(P0.01)。Transwell实验结果显示A549-siTCF3和H1299-siTCF3细胞迁移数显著低于A549-NCsiRNA和H1299-NCsiRNA组细胞(P0.05)。流式细胞术分析结果显示A549-siTCF3细胞和H1299-siTCF3细胞的凋亡率显著高于A549-NCsiRNA和H1299-NCsiRNA细胞(P0.01)。Western blot实验结果显示,下调TCF3表达能抑制Wnt蛋白的表达,MMP-9和MMP-13的蛋白表达明显降低,TIMP-1的蛋白表达增高。结论:siTCF3显著抑制A549细胞和H1299细胞的增殖和迁移能力,并诱导细胞凋亡,其分子机制可能通过下调Wnt通路活性以及调控MMP家族关键成员的表达而实现。     

慢病毒靶向携带survivin-siRNA抗肺腺癌裸鼠体内研究

目的探讨慢病毒载体介导survivin-siRNA对人肺腺癌裸鼠移植瘤的体内抑瘤活性。方法参考siRNA的设计策略,构建表达survivin-siRNA的慢病毒载体;于各BALB/C裸鼠右侧腋窝皮下接种人肺腺癌A549细胞悬液,构建人肺腺癌A549细胞裸鼠移植瘤模型,肿瘤组织局部注射survivin-siRNA的慢病毒载体,观察肿瘤的体积及随时间变化的生长曲线;通过碘化丙啶(propidiumiodide,PI)染色检测细胞凋亡情况;流式细胞术检测肿瘤细胞周期变化。结果慢病毒载体介导survivin-siRNA对裸鼠人肺腺癌A549的抑瘤率为46.07%;经过PI和Annexin-V染色区分凋亡早晚期的细胞为30%~35%,荧光显微镜下观察肿瘤细胞凋亡;G1期细胞比例明显增加,S期细胞比例则明显减少。结论慢病毒载体介导的siRNA能有效抑制裸鼠移植人肺腺癌A549的survivin基因的表达,有效激发细胞凋亡。     

Inhibition of VEGFR2 prevents DMBA-induced mammary tumor formation

Preinvasive mammary pathologies in humans and rat chemical carcinogenesis model systems have an increased microvascular density relative to normal tissue. This suggests the possibility of preventing invasive breast cancer by inhibiting angiogenesis. Vascular endothelial cell growth factor (VEGF) is a potent angiogenic growth factor, commonly involved in tumor-induced angiogenesis. Here, we show that both VEGF and VEGFR2 expression increase with histological progression to invasive disease in the rat 7,12-dimethylbenz[a]anthracene (DMBA) model. Other VEGF receptors, VEGFR1, neuropilin 1 and neuropilin 2, are constitutively expressed throughout progression. To examine whether VEGF signaling is functionally relevant to tumor-induced endothelial tubule formation in vitro and for tumor formation in vivo, we utilized the VEGFR2 inhibitor, ZD6474. In vitro endothelial cell tubulogenesis induced by isolated mammary organoids or carcinoma in situ from DMBA-treated rats is inhibited by ZD6474, in a dose-dependent fashion. The administration of ZD6474 to DMBA-treated rats inhibits the formation of atypical ductal hyperplasia and carcinoma in situ by greater than 95% (P < 0.05), when administered 1 week or 6 weeks post-DMBA initiation. Invasive disease was absent in all ZD6474 cohorts. These data support the hypothesis that progression of DMBA-induced preinvasive mammary pathologies to palpable disease requires angiogenesis via a VEGF-dependent mechanism.     

黄芪注射液对H22肝瘤小鼠的抑瘤作用及免疫功能的影响

目的:研究黄芪注射液对小鼠H22移植瘤的生长抑制作用及免疫功能的影响。方法:采用移植性H22肝癌小鼠模型,随机分为模型对照组,5-Fu处理组,黄芪注射液高、中、低剂量组。分别连续腹腔注射5-Fu(25 mg.kg-1),黄芪注射液(12 g.kg-1、8g.kg-1和4g.kg-1)10 d后,处死小鼠,计算抑瘤率、外周血白细胞数、脾指数、胸腺指数I、L-2、TNF-α等指标,分析黄芪注射液对小鼠H22移植瘤的生长抑制作用及免疫功能的影响。结果:与模型组相比,黄芪注射液低、中、高剂量组能显著减少移植瘤瘤重,其抑瘤率分别为18.23%,31.49%,43.09%,其中黄芪注射液高剂量组与CTX组抑瘤率比较,抑瘤率有显著性差异(P<0.05)。黄芪注射液各组可不同程度地升高荷瘤小鼠的白细胞数和胸腺指数、脾指数,且能提高荷瘤小鼠血清中IL-2和TNF-α的水平(P<0.05)。结论:黄芪注射液对小鼠H22移植瘤具有明显的抑瘤作用,其作用可能与增强机体的免疫功能有关。     

PRIMA-1(MET) inhibits growth of mouse tumors carrying mutant p53

Reactivation of the tumor suppressor activity to mutant p53 should trigger massive apoptosis and eliminate tumors. The low molecular weight compounds PRIMA-1 and the structural analog PRIMA-1(MET) reactivate human mutant p53 in vitro and suppress growth of human tumor xenografts in SCID mice. However, little is known about their effect on mouse mutant p53 in mouse tumor cells. We have examined the effect of PRIMA-1(MET) on mouse sarcomas, mammary carcinomas and chemically induced fibrosarcomas. PRIMA-1(MET) showed potent growth suppression in mutant p53-carrying mouse tumors in vitro and a significant anti-tumor effect in syngeneic mice in vivo. These results demonstrate that PRIMA-1(MET) targets mouse tumors carrying mutant p53 and provide strong support for the anti-tumor efficiency of PRIMA-1(MET) in vivo.     

Extraction and Isolation of Alkaloids of Sophora Alopecuroides and Their Anti-Tumor Effects in H22 Tumor-Bearing Mice

Background

Alkaloids of Sophora alopecuroides have good biological activity, and are widely used in clinical settings, which not only have pharmacological activities of anti-cancer, cancer suppression, as well as the inhibition, and killing of various microorganisms; but also possess extensive pharmacological effects on immune system, nervous system and cardiovascular system. The objective of this paper was to extract and isolate total alkaloids of Sophora alopecuroides (TASA), and to study their anti-tumor effects in H22 tumor-bearing mice.

Materials and Methods

TASA were extracted and isolated using thin-layer chromatography, and column chromatography; and the isolated compounds were analyzed using nuclear magnetic resonance. The inhibitory effects of TASA on tumor in H22-bearing mice were determined by MTT assay.

Results

Three compounds were isolated from Sophora alopecuroides L., which were matrine, oxymatrine and sophoridine, respectively. Meanwhile, mouse H22 sarcoma model was established and different doses of TASA apparently inhibited solid H22-tumor in mice; it inhibited the thymus, and spleen to some extent; the degree of inhibition was more obvious for the spleen.

Conclusion

TASA has an anti-tumor effect in H22 tumor-bearing mice.     

Augmentation of anti-tumor activity by immunization with Mycobacterium tuberculosis (Tbc) and tuberculin-coupled tumor cells

The anti-tumor effect of immunization with heat-killed Mycobacterium tuberculosis (Tbc) and Tuberculin (PPD)-coupled syngeneic tumor cells was examined in vivo. Three tumor cell lines were employed. Immunization of Tbc-primed BALB/c mice with PPD-coupled syngeneic Meth-A tumor cells displayed a potent anti-tumor effect on viable Meth-A cells inoculated subcutaneously. Neither PPD-coupled LLC (Lewis Lung Carcinoma) cells nor sonicated PPD-coupled Meth-A cells were capable of immunizing these mice. PPD-coupled syngeneic whole tumor cells were indispensable for induction of this tumor-specific resistance. Immunization of Tbc-primed C3H/He mice with PPD-coupled syngeneic MH134 tumor cells did not elicit anti-tumor activity against MH134, but additional pretreatment of mice with cyclophosphamide brought on an anti-tumor effect. Antimetastatic reactivity was investigated in C57BL/6 mice bearing LLC, with a reduction in metastases noted. This antimetastatic effect was observed even when the mice were immunized with PPD-coupled LLC cells three days after removal of the initial tumor. Immunization with Tbc and PPD-coupled Meth-A cells together with intraperitoneal administration of murine or rat interleukin 2 (IL 2) further augmented anti-Meth-A resistance. Murine IL 2 further inhibited tumor growth during the early stage, while rat IL 2 showed an anti-tumor effect throughout the course of tumor growth.     

Inhibition of tumor growth by peptide specific cytotoxic T lymphocytes in a three-dimensional collagen matrix

Tumor associated, MHC I restricted antigenic peptides have been identified in both human and mouse tumors. Cytotoxic T lymphocytes (CTL) which recognize these tumor associated antigenic peptides are potential anti-cancer effectors. The anti-tumor activity of CTL is usually measured in vitro by the ⁵¹Cr release assay and in mice by tumor growth inhibition which is the most direct assessment of anti-tumor effect. In clinical studies, an in vivo tumor growth inhibition assay is not an option and an in vitro assay which corroborates with in vivo tumor growth is needed to assess the long-term outcome of CTL activity. Here, a three-dimensional (3-D) collagen gel assay was developed to measure in vitro the inhibition of mouse mammary tumor growth by anti-tumor CTL. BALB/c mouse CTL were induced with peptide E474 SFAVATTAL which was expressed by mouse mammary tumor cells D2F2. To measure D2F2 tumor growth inhibition in vitro, a mixture of tumor cells and anti-E474 CTL in a 1 μl cell bolus was embedded in the collagen gel. Complete eradication of tumor growth was observed at E:T ratio of or greater than 1:1. rIL-2 supplementation was necessary to achieve long-term tumor growth inhibition. Even spontaneous D2 tumor explant could be grown in the collagen gel and addition of anti-E474 to this culture reduced tumor growth. This assay system provides a realistic and sensitive alternative to the in vivo tumor growth inhibition assay and allows easy adaptation to test additional therapeutic reagents.     

Effects of AZD2171 and vandetanib (ZD6474, Zactima) on haemodynamic variables in an SW620 human colon tumour model: an investigation using dynamic contrast-enhanced MRI and the rapid clearance blood pool contrast agent, P792 (gadomelitol)

The effect of two novel therapeutic agents on tumour haemodynamics was investigated using a fast dynamic contrast-enhanced (DCE)-MRI protocol (0.5 s/image) sensitive to signal changes in both the vascular input function and tumour during the administration of the macromolecular rapid clearance blood pool agent (MM-RCBPA), gadomelitol (P792, Vistarem). This enabled simultaneous measurement of the tumour blood flow per unit volume of tissue (F/V(T), mL/s/mL), the fractional plasma volume (V(p), %), and the permeability surface area product per unit volume of tissue (PSrho, s(-1)) in subcutaneous SW620 human colorectal tumour xenografts grown in nude rats before and after (at 0 and 22 h; imaging at 24 h) acute treatment with AZD2171 (3 mg/kg) and vandetanib (ZD6474, Zactima; 50 mg/kg), which have inhibitory activity against vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase. MRI was performed at 4.7 T using a single-slice, modified, T(1)-weighted, spoiled gradient-echo technique. Both compounds reduced gadomelitol uptake into the tumour. AZD2171 and vandetanib, respectively, (a) greatly reduced PSrho to 19.7 +/- 9.5% and 28.9 +/- 14.1% of baseline (P = 0.007 and P = 0.02), (b) markedly reduced V(p) to 31.2 +/- 19.1% and 54.8 +/- 21.2% of baseline (P = 0.015 and P = 0.09), and (c) had no significant effect on F/V(T). There was no significant difference between groups treated with AZD2171 and vandetanib when each variable was compared. The reductions in PSrho and V(p) are consistent with inhibition of VEGF signalling. AZD2171 (3 mg/kg) and vandetanib (50 mg/kg) were also found to produce a comparable chronic inhibition of SW620 tumour growth (89% for both). This study shows that DCE-MRI using an MM-RCPBA can be used to distinguish tumour vascular flow, volume, and permeability surface area product in a tumour model, and enables the acute effects of VEGF signalling inhibition to be examined in detail.     

Synthesis and evaluation of 1-benzhydryl-sulfonyl-piperazine derivatives as inhibitors of tumor growth and tumor angiogenesis of mouse ehrlich ascites tumor in vivo

A series of novel 1-benzhydryl-sulfonyl-piperazine derivatives 3(a-e) were synthesized by nucleophilic substitution reaction of 1-benzhydryl-piperazine with different sulfonyl chlorides and were characterized by 1H NMR, LC/MS, FTIR and elemental analysis. In the present study, the compounds 3(a-e) exhibited in vivo inhibition of Ehrlich ascites tumor (EAT) cell growth and increased the Median Survival Time (MST) and %ILS of EAT bearing mice. Further treatment of derivatives in vivo resulted in reduction of EAT cell number and ascites formation. The efficacy of the derivatives to inhibit the angiogenesis in vivo was evaluated in tumor bearing mice peritoneum and chorio allantoic membrane (CAM) model. The compounds suppressed the blood vessel formation in vivo in mice peritoneum and in CAM. Among the compounds studied, 3e demonstrated highest tumor inhibitory and anti-angiogenic effects against mouse tumor. However, this phenomenon needs detailed investigation.     

阿司匹林-烟酰胺-锌络合物荷H22肝癌小鼠作用的研究

目的：研究阿司匹林-烟酰胺-锌络合物（商品名：佛立沙,wuY）抗肿瘤作用。方法：在小鼠腋皮下接种H22肿瘤细胞后,每日igwUY1次,连续给药9d,第10d处死小鼠,剥取瘤块称重并计算抑瘤率。结果：wUY40mg·kg-1对小鼠H22抑制率为32．83％,与模型组比较,wUY有显著的抑制小鼠H22移植瘤的作用（P〈0．05）,结论：wUY对小鼠H22移植瘤有明显的抑制作用。     

黄芪多糖对荷瘤小鼠IL-2、IL-6、IL-12和TNF-α水平的影响

目的：研究黄芪多糖对荷瘤小鼠肿瘤生长及细胞因子水平的影响。方法：建立小鼠肝癌H22和小鼠肉瘤S180移植性肿瘤模型,检测黄芪多糖的体内抗肿瘤活性;采用ELISA法检测黄芪多糖对荷瘤小鼠血清中白细胞介素-2（IL-2）、白细胞介素-6（IL-6）、白细胞介素-12（IL-12）、肿瘤坏死因子-α（TNF-α）水平的影响。结果：黄芪多糖在50,100mg·kg^-1时,对小鼠肝癌H22的抑瘤率分别为32．84％,45．09％,对小鼠肉瘤S180的押瘤率分别为36．55％,50．35％,且能提高荷瘤小鼠的脾指数和胸腺指数;黄芪多糖能提高荷瘤小鼠血清中细胞因子IL-2、IL-6、IL-12和TNF-α的水平。结论：黄芪多糖具有明显的体内抗肿瘤活性,其机制可能与增强机体的免疫功能有关。