Inhibitory Effects of Ginsenoside Rb1 on Apoptosis Caused by HSV-1 in Human Glioma Cells

To investigate the inhibitory effects of Ginsenoside Rbl （GRbl） on apoptosis caused by Herpes Simplex Virus-1 （HSV-1） in Human Glioma Cells （U251）, U251 cells were infected by HSV-1 at a multiplicity of infection of 5 and GRbl, GRbl＋HSV-1, HSV-1 and control groups. MTT and cell apoptosis assays were used to detect the inhibitory effects of GRbl on the apoptosis of U251 cells that caused by HSV-1 infection for various concentrations of drug and virus treatments by MTT assay. We found that in the 400 μg/mL GRb 1 and 400 μg/mL GRbl＋HSV-1 groups, MTT values were higher than control group at all times （P〈0.05）. Moreover, the apoptosis rate in the 400 μg/mL GRbl＋HSV-1 group was lower than the HSV-1 group （P〈0. 05）. These results confirmed that, at appropriate concentrations, GRbl could inhibit nerve cell apoptosis in HSV-1 infections.

Activation of CD40 by Soluble Recombinant Human CD40 Ligand Inhibits Human Glioma Cells Proliferation via Nuclear Factor-κB Signaling Pathway

As CD40 transduces activation signals involved in inflammatory and immune disorders,we explored the expression and response to CD40 engagement in human glioma cell lines in this study.The CD40 expression in BT-325 and U251 cells was flow cytometrically detected.The cells were incubated with srhCD40L for 72 h to assess its effects on cell growth in vitro.TNF-α expression was quantified by real-time PCR,and protein expression was analyzed by ELISA.The I-κb mRNA was detected by RT-PCR.I-κB expression decreased after stimulation with 1 μg/mL srhCD40L,but it was upregulated after the cells were pretreated with CD40 antibody.srhCD40L significantly inhibited the proliferation of the CD40+ human glioma cells.The stimulation of CD40+ glioma cells with soluble CD40L (CD154) up-regulated the expression of TNF-α at both mRNA and protein levels.We are led to conclude that CD40L/CD40 could inhibit human glioma cells through I-κb signaling pathway.Interferon-γ can augment CD40 expression and the inhibitory effect of CD40 ligand on cell growth in vitro.These results suggest that srhCD40L may benefit the therapy strategy of glioma.

THE STUDIES ON MONOCLONAL ANTIBODY SZ-39 AGAINST HUMAN GLIOMA CELLS

A hybridoma cell line SZ-39 secreting monoclonal antibody against the human glioma cell has been established by a fusion between NS-1 myeloma cells and spleen cells from mice immunized with human glioma cell lines. Monoclonal antibody (McAb) SZ-39 was analyzed by ELISA, quantitative absorption, indirect immunofluorescence and ABC immunohistology. McAb SZ-39 strongly bound to 9/10 glioma cell lines, 17/20 glioma tissues, weakly bound to one liver cancer cell line and 1/2 lung cancer line, but they did not band with other tested human cancer linse. NcAb SZ-39 have no cross-reaction with lymphocyte, ABC red blood cells, white blood cells, blood platelet, normal bone marrow cells, fibroblast cells and 12 normal human tissues.The result indicated the antigen recognized by McAb SZ-39 may be a glioma-associated antigen <GAA). This GAA was analyzed by means of Western blotting. It was a MW 180 Kd glycopro-tein. The 131I-McAb SZ-39 specifically localized in human glioma xenografted in nude mice that indicate it may be useful in radioimmunoimaging and as a target for immunotherapy on human glioma.

Adiponectin Supports Human Glioma Cells Survival against Temozolomide through Enhancement of Autophagic Response in Glioma Cells

Objective: To investigate the role of adiponectin in human glioma cell lines against the temozolomide and the molecular regulation mechanism. Methods: Human glioma cell lines U251 and U-87MG were cultured in Dulbecco’s modified eagle medium (DMEM) containing 4500 mg/L glucose. MTT was used to measure cell growth ratio. Western blot was used to detect the protein levels of autophagy-related protein (Beclin 1, LC3 I/II, p62) and phosphorylated AMPK (p-AMPK) in human glioma cell lines. After AICAR and Compound C were administered, the change of p-AMPK and the autophagy level were examined by western blot. Results: While adiponectin stimulates AMPK in phosphatase and up-regulates the level of autophagy, human glioma cell lines obtain more resistance against the temozolomide, which is facilitated by AICAR and weakened by Compound C. Conclusion: As an important adipokine, adiponectin can up-regulate the glioma cell autophagy by activating the AMPK signaling pathway which increases the resistance of glioma cells to temozolomide.

The influence of small interfering RNA on the expression of Survivin in human glioma cells

Objective This study aims to investigate the feasibility of knockdown of Survivin gene with small interfering RNA and to observe the apoptosis in gliomas which is influenced by siRNA. Methods Survivin specific siRNA oligonucleotides were designed and synthesized artificially. This siRNA

DAPT suppresses the proliferation of human glioma cell line SHG-44

Objective:To explore the suppressing effect ofγ-secretase inhibitor DAPT on proliferation of human glioma cell line SHG-44 in vitro and its mechanism.Methods:The SHG-44 cell was treated by DAPT with different concentration.The proliferation of cells was detected by MTT assay;cell cycle and TSC of CD133^+were determined by flow cytometry analysis technique;the key factor in Notch signaling pathway(Notch-1,Delta-1,Hes-1)was measured by reverse transcrip tase-polymerase chain reaction and western blotting.Results:DAPT inhibited the growth and proliferation of SHG-44 cells significantly(P<0.05).And the inhibiting effect on SHG-44 cells produced by DAPT showed a dose-dependent manner.DAPT increased the rate of cells in G_0/G_1 phase of SHG-44 cells,while it decreased the rate of cells in S phase.TSC of CD133^+was significantly reduced after DAPT treated SHC-44 cells.The expression of protein and mRNA of Notch-1,Delta-1 and Hes-1 were gradually downregulated with the increase of DAPT doses.Conclusions:DAPT can downregulate these key factor in Notch signaling pathway,reduce the TSC of CD133+and inhibit the proliferation of SHC-44 cells.

Radio-resistance induced by nitric oxide to heavy ion irradiation in A172 human glioma cells

To investigate effects of nitric oxide on cellular radio-sensitivity, three human glioma cell lines, i.e. A172, A172 transfected green fluorescence protein (EGFP) gene (EA172) and A172 transfected inducible nitric oxide synthesis (iNOS) gene (iA172), were irradiated by 12C6+ ions to 0, 1 or 2Gy. Productions of nitric oxide and glutathione (GSH) in A172, EA172 and iA172 were determined by chemical methods, cell cycle was analyzed by flow cytometry at the 24th hour after irradiation, and survival fraction of the cells was measured by colorimetric MTT assay at the 5th day after irradiation. The results showed that the concentrations of nitric oxide and GSH in iA172 were significantly higher than in A172 and EA172; the G2/M stage arrest induced by the 12C6+ ion irradiation was observed in A172 and EA172 but not in iA172 at the 24th hour after exposure; and the survival fraction of iA172 was higher than that of EA172 and iA172. Data suggest that the radio-sensitivity of the A172 was reduced after the iNOS gene transfection. The increase of GSH production and the change of cellular signals such as the cell cycle control induced by nitric oxide may be involved in this radio-resistance.

Antitumor effect of tumor necrosis factor-related apoptosis inducing ligand combined with mevastatin on a human glioma cell line SWO-38

BACKGROUND： Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor necrosis factor-related apoptosis inducing ligand （TRAIL）. OBJECTIVE： To explore the effect of TRAIL combined with mevastatin on the proliferation and apoptotic cell death of a human glioma cell line SWO-38, and to study its mechanism of action. DESIGN, TIME AND SETTING： An in vitro control experiment was performed at the Central Laboratory of the Third Hospital Affiliated to Sun Yat-sen University, between January and April 2009. MATERIALS： The human SWO-38 cell line was provided by Cell Research, Department of Animal Experimental Center of Sun Yat-sen University; human recombinant soluble TRAIL by R＆D, USA; and mevastatin by Sigma, USA. METHODS： SWO-38 cells were separately incubated in TRAIL （100, 200, 300, 400, and 500 tJg/L） and mevastatin （5, 10, 20, 30, and 40 pmol/L） for 72 hours. In addition, SWO-38 cells were incubated in TRAIL （300 μg/L）, mevastatin （30 μmol/L）, and a solution containing both TRAIL and mevastatin for 12, 24, 48 and 72 hours. MAIN OUTCOME MEASURES： Cell proliferation was detected using methyl thiazolyl tetrazolium assay; cell apoptosis was observed using Hoechst 33258 staining and fluorescence microscopy and was measured using Annexin V/propidium iodide flow cytometry; TRAIL R1/DR4 and TRAIL R2/DR5 protein expressions levels were measured using indirect immunofluorescence staining combined with flow cytometry in the recombinant soluble TRAIL （rsTRAIL, 300 tJg/L）, mevastatin （30 IJmol/L） and combination groups; TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression was detected using real-time polymerase chain reaction. RESULTS： rsTRAIL, mevastatin and their combination inhibited tumor proliferation in a time- and dose-dependent manner. The proliferation inhibitory rate and apoptosis rate of human SWO-38 cells in the combined group were significantly greater than the rsTRAIL or mevastatin alone group （P 〈 0.01）. TRAIL R1/DR4 and TRAIL R2/DR5 protein and mRNA expressions were increased in the combination group compared with mevastatin or rsTRAIL alone after 72 hours （P 〈 0.01）. CONCLUSION： Both rsTRAIL and mevastatin inhibit the proliferation and apoptosis of the human glioma cell line SWO-38, while their combination enhances the anti-tumor effect. The mechanism of action possibly correlates to the upregulation of TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression by mevastatin, thereby enhancing the cell sensitivity to rsTRAIL.

Inhibition of epidermal growth factor receptor signaling protects human malignant glioma cells from hypoxia - induced cell death

Epidermal growth factor receptor(EGFR)signaling has become an importanttarget for drug development becauseEGFR signaling enhances tumor cell proliferation,migration,and invasion and inhibits apoptosis.However,theresults of clinical trials using EGFR inhibitors in patients with solid tumors have been disappointing.Here,wereport a protective effect of the EGFR inhibitors AG1478 and PD153035 against cell death induced by acute hy-poxia,which contrasts with their proapoptotic effects under normoxia.Under hypoxic conditions,both agents re-

咖啡因通过FAK/AKT/ROCK通路调控人脑胶质瘤U-373MG细胞的恶性生物学行为

目的:探讨咖啡因通过调节FAK/AKT/ROCK信号通路来影响人脑胶质瘤U-373MG细胞的增殖、迁移和侵袭能力。方法:常规培养U-373MG细胞,将其分为对照组、咖啡因低剂量(1 mmol/L)组、咖啡因高剂量(2 mmol/L)组、PF573228组(FAK抑制剂,1μmol/L)、咖啡因高剂量+SC79组(AKT激活剂,8mg/L)。用CCK-8法、Transwell小室实验、流式细胞术和WB法分别检测各组U-373MG细胞的增殖、迁移、侵袭及凋亡,以及U-373MG细胞中p-FAK、p-AKT、p-ROCK、Ki67、MMP-9蛋白表达水平。建立U-373MG细胞裸鼠移植瘤模型,观察咖啡因对移植瘤生长的影响,WB法检测移植瘤组织中相关蛋白的表达。结果:咖啡因、PF573228可显著抑制U-373MG细胞的增殖、迁移、侵袭能力,促进U-373MG细胞凋亡,抑制p-FAK、p-AKT、p-ROCK、Ki67、MMP-9蛋白的表达(均P<0.05),SC79则可部分逆转咖啡因对U-373MG细胞的作用(均P<0.05)。咖啡因可显著抑制移植瘤的生长及移植瘤组织中上述相关蛋白的表达(均P<0.05)。结论:咖啡因可通过抑制FAK/AKT/ROCK信号通路抑制U-373MG细胞的增殖、迁移和侵袭能力,并促进其凋亡。

hUMSCs外分泌上清联合替莫唑胺在不同胶质瘤细胞系中的协同增敏作用

目的:探讨人脐带间充质干细胞外分泌上清(hUMSC-CM)联合替莫唑胺(TMZ)在不同胶质瘤细胞系中的协同增敏作用及潜在机制。方法:采用2种血清剥夺法(24和48 h分批次撤血清法)收集hUMSC-CM并制备成冻干粉,设置5种浓度(0、1、3、6和9 g/L)处理大鼠恶性胶质瘤细胞系RG-2、人星形细胞瘤细胞系U251和人胶质母细胞瘤细胞系LN-428。通过CCK-8实验检测hUMSC-CM作用于胶质瘤细胞24、48和72 h后的肿瘤抑制可行性及敏感度。HE染色结合CCK-8法确定6种浓度(0、25、50、100、200和400µmol/L)的TMZ作用于胶质瘤细胞48 h后化疗敏感性的差异。筛选出低、高2种浓度(3和9 g/L)的hUMSC-CM和低、中、高3种浓度(50、100和200µmol/L)的TMZ配伍,作用于胶质瘤细胞后检测细胞活力和病理形态学变化。TUNEL染色检测细胞凋亡;流式细胞术分析细胞周期变化;Western blot检测凋亡相关蛋白cleaved caspase-3、cleaved caspase-8和cleaved PARP1,以及自噬相关蛋白beclin-1和LC3的表达变化,探讨hUMSC-CM与TMZ体外联合给药协同增敏的作用机制。结果:3种胶质瘤细胞系对hUMSC-CM和TMZ的敏感度为RG-2>U251>LN-428。hUMSC-CM(3和9 g/L)与TMZ(50、100和200µmol/L)配伍给药对胶质瘤细胞生长的抑制作用比单独给药组显著增强(P<0.05),且随着配伍药物剂量的增加而增强。其中,9 g/L hUMSC-CM(C9)与50µmol/L TMZ(T50)配伍可有效抑制胶质瘤细胞生长。与C9或T50组相比,CCK-8实验显示C9+T50组细胞活力显著下降(P<0.05),HE染色和TUNEL检测结果显示C9+T50组细胞形态变化明显,出现典型凋亡形态学特征,流式细胞术结果显示C9+T50可诱导胶质瘤细胞周期发生阻滞,Western blot结果显示C9+T50组细胞中cleaved caspase-3、cleaved caspase-8、cleaved PARP1、beclin-1和LC3-II/LC3-I水平显著升高(P<0.01)。结论:(1)hUMSC-CM与TMZ配伍给药对胶质瘤细胞的抑制作用具有广谱性,且两者之间存在增敏作用,在不同细胞系中呈现不同的增敏效果。(2)hUMSC-CM提高胶质瘤细胞对TMZ敏感度的机制可能与调节caspase-8/caspase-3/PARP1信号通路及自噬通路、诱导胶质瘤细胞发生凋亡和自噬有关。

姜黄素通过改变FAK表达和激活caspase诱导人脑胶质瘤U251细胞凋亡

目的研究姜黄素诱导U251细胞凋亡机制。方法20～100μmol·L^-1姜黄素分别处理U251细胞24h后，MTT法测定姜黄素对U251细胞的细胞抑制作用及各种caspase抑制剂对姜黄素作用的影响；通过流式细胞仪检测细胞凋亡；透射电镜观察细胞形态学变化；用免疫细胞化学分析姜黄素对FAK（focal adhesion kinase，粘着斑激酶）蛋白质表达的影响；荧光分光光度法检测caspase-3活性的改变。结果姜黄素明显抑制U251细胞的增殖；诱导U251细胞凋亡；FAK蛋白表达减少；easpase-3活性增强，各种caspase抑制剂可抑制姜黄素诱导的U251细胞凋亡。结论姜黄素通过抑制FAK蛋白的表达和激活caspase途径可诱导U251细胞凋亡。

葛根素对胶质瘤细胞迁移侵袭能力影响研究

目的:探讨葛根素对人胶质瘤细胞U251的迁移、侵袭能力的影响。方法:体外培养U251细胞,加入佛波脂诱导,明胶酶谱法和Transwell小室分别观察不同浓度葛根素对其MMP表达水平及迁移侵袭能力的影响。结果:与对照组相比,葛根素显著降低U251细胞的MMP-2、MMP-3、MMP-9酶活性及迁移、侵袭能力,且呈一定量效关系。结论:通过抑制MMP酶活性,葛根素可有效抑制人胶质瘤细胞U251的迁移侵袭。

NGF及其活化受体p-TrkA在人脑胶质瘤细胞株U251细胞周期中的多靶点分布模式

为了探讨神经生长因子(NGF)及其活化受体磷酸化的酪氨酸蛋白激酶A(p-TrkA)在人脑胶质瘤细胞株U251细胞周期中的多靶点分布模式及其生物学意义,采用免疫荧光双标记技术对处于细胞周期不同时相细胞内的NGF和p-TrkA的动态分布进行亚细胞定位,并观察了抗癌药物羟基脲、紫杉醇和秋水仙素及抗NGF-β中和血清对NGF和p-TrkA在细胞分布的影响;用免疫印迹技术检测细胞核和细胞质内NGF和p-TrkA的相对含量以及细胞培养液内的分泌性NGF。免疫荧光染色结果表明:分裂相细胞在重新贴壁生长6h后,NGF主要分布于核周区,p-TrkA主要定位于细胞膜;培养12h后,NGF和p-TrkA共同转位至细胞核内;在M期,NGF主要定位于中心体,p-TrkA主要定位于纺锤丝;用羟基脲将细胞阻滞于G1/S期后,NGF和p-TrkA主要积聚在细胞核内;用紫杉醇或秋水仙素处理后,NGF与γ-Tubulin仍然共定位于中心体,p-TrkA与α-Tubulin共定位于异形纺锤丝上或弥散分布于细胞质内。用兔抗人NGF-β抗血清中和培养基中分泌性的NGF后,细胞内NGF和p-TrkA免疫荧光强度明显减弱。免疫印迹结果显示:G1/S期细胞核内的NGF和p-TrkA蛋白条带明显浓于细胞质内的蛋白条带。上述结果提示:人脑胶质瘤U251细胞高表达NGF及其高亲和力受体TrkA,并将NGF分泌至细胞外;胞外NGF与细胞膜上TrkA结合后形成NGF/p-TrkA复合物内化入胞内;NGF/p-TrkA在细胞内的分布具有细胞周期性特征;NGF/p-TrkA可通过多靶点作用模式调控U251细胞的生物学行为。上述多靶点分布模式为研制NGF修饰的抗肿瘤靶向药物提供了细胞生物学基础。

CpG ODN107增强人脑胶质瘤细胞放射敏感性的研究

目的:探讨CpG ODN107增加人脑胶质瘤细胞CHG-5放射敏感性的作用及可能机制。方法:用不同浓度CpG ODN107处理CHG-5细胞,然后经β射线照射,MTT法检测细胞的增殖情况,体外培养集落形成率与细胞划痕法观察细胞的集落形成和迁移能力,ELISA法检测细胞TNF-α的分泌水平。结果:CpG ODN107抑制CHG-5细胞的增殖,并呈量效关系。CpG ODN107(10μg/ml)联合β射线照射,抑制CHG-5细胞的增殖作用最强。CpG ODN107(10μg/ml)同样能抑制CHG-5细胞增殖和迁移,并且增加了TNF-α的分泌,在联合β射线照射后作用更加显著。结论:CpG ODN107对CHG-5有明显的放射增敏作用,其机制可能与CpG ODN107增强肿瘤细胞TNF-α的分泌有关。

共刺激分子4-1BBL和B7-1在人脑胶质瘤细胞中的表达

背景与目的:4-1BBL和B7-1为诱导和维持T细胞活化提供了重要的共刺激信号,目前被认为是提高抗肿瘤免疫的治疗靶点。本研究探讨4-BBL和B7-1在7株胶质瘤细胞系表面的表达情况。方法:用流式细胞仪检测7株胶质瘤细胞株表面的共刺激分子4-1BBL和B7-1的表达,同时用MTT法分析胶质瘤细胞系对抗癌药物长春新碱(VCR)敏感性,并分析4-1BBL的表达与耐药性的相关性。结果:发现在所检测的胶质瘤细胞表面有不同程度的表达4-1BBL,但均不表达B7-1。其中T98G和MGR1细胞表面的4-1BBL表达>30%,对VCR不敏感,UW28、SKMG1、MGR2、SF767、SKMG4细胞表面的4-1BBL表达<10%,对VCR敏感。结论:本研究所检测的胶质瘤细胞均不表达共刺激分子B7-1,但有不同程度的表达4-1BBL,并且4-1BBL高表达的胶质瘤细胞对长春新碱敏感性差。

鹿茸多肽对人胶质瘤细胞生长抑制率及细胞周期的影响

目的观察鹿茸多肽对人胶质瘤细胞生长抑制率及细胞周期的影响,探讨鹿茸多肽抑制肿瘤细胞的增殖及调节细胞周期作用的机制。方法在体外传代的培养人胶质瘤细胞(U251)细胞株中加入不同浓度(50、100、200、400、800μg/mL)的鹿茸多肽,诱导培养48 h,镜下观察细胞的形态学变化,MTT法检测鹿茸多肽对肿瘤细胞增殖情况,计算抑制率;流式细胞术(FCM)分析鹿茸多肽,诱导培养肿瘤细胞48 h后,细胞周期变化情况。结果形态学观察表明,与对照组相比,随着药物剂量的增加,实验组细胞密度逐渐降低,细胞间隙逐渐增宽,细胞体积逐渐缩小,细胞内颗粒逐渐增多。MTT法检测结果表明,鹿茸多肽对肿瘤细胞的增殖抑制作用明显,细胞生长抑制率随着剂量增加抑制率逐渐增加,呈现出良好的剂量依赖性。FCM检测表明,肿瘤细胞G0/G1期与S期所占百分比逐渐减少,G2/M期阻滞。48 h均出现凋亡峰,及凋亡细胞群。结论鹿茸多肽对体外培养的人胶质瘤细胞的增殖有抑制作用,并具有量效关系。可使肿瘤细胞阻滞在细胞周期的G2/M期,继而引起的细胞周期阻滞和诱导其凋亡。

钩吻素子对神经胶质瘤细胞U251生长抑制及诱导凋亡作用

目的:探讨钩吻素子体外对神经胶质瘤细胞U251的生长抑制作用及诱导凋亡的作用.方法:利用MTT法和台盼蓝拒染法观察钩吻素子对神经胶质瘤细胞U251生长抑制作用.应用激光共聚焦、流式细胞仪、电子显微镜检测钩吻素子诱导U251细胞的凋亡作用.结果:MTT结果显示钩吻素子在(5～50mg/L)的浓度范围内对人神经胶质瘤U251细胞具有显著的抑制作用.生长曲线结果显示药物的各个浓度对U251的抑制作用呈时间依赖性.流式细胞仪可以观察到明显的"亚G1期"峰(凋亡峰),且凋亡率达到22.4%.激光共聚焦显微镜可以观察到典型的凋亡核形,如核固缩和核碎裂等.透射电子显微镜下见到典型的早期凋亡形态学表现.结论:在一定的浓度范围内,钩吻素子可以抑制U251细胞的生长,并呈剂量和时间依赖效应.其抗肿瘤的特性与引起肿瘤细胞的凋亡有关.

蒿甲醚自微乳化给药系统对小鼠人脑胶质瘤皮下移植瘤的抑瘤作用研究

目的:研究蒿甲醚(ARM)自微乳化给药系统(SMEDDS)对人脑胶质瘤皮下移植瘤模型小鼠的抑瘤效果。方法:以人脑胶质细胞瘤细胞株SHG44接种,并以组织块移植传代,建立裸小鼠皮下移植瘤模型。分别于接种后的第5、10、15、20、25天时测量小鼠肿瘤组织体积,绘制肿瘤生长曲线,确定肿瘤快速增殖初期。取裸小鼠30只,同法建立皮下移植瘤模型,并于肿瘤快速增殖初期时分为对照组(生理盐水)、ARM混悬液组[60 mg/(kg·d)]和ARM-SMEDDS低、中、高剂量组[10、20、30 mg/(kg·d)]并灌胃给予生理盐水或相应药液,每日1次,连续给药30 d。记录小鼠体质量变化及一般情况,测定肿瘤组织体积变化并计算相对肿瘤增殖率。结果:皮下移植肿瘤块组织后第10天左右即进入肿瘤快速增殖初期。给药期间各组小鼠一般情况正常,未见明显异常反应。自给药第10天起,ARM-SMEDDS各剂量组小鼠的肿瘤组织体积均较对照组显著缩小(P<0.05);自给药第15天起,ARM-SMEDDS各剂量组小鼠的肿瘤组织体积均较ARM混悬液组显著缩小(P<0.05)。末次给药后,ARM-SMEDDS各剂量组小鼠的相对肿瘤增殖率均较ARM混悬液组均显著降低(P<0.05)。结论:ARM-SMEDDS具有明显的抑制人脑胶质瘤增长的效果,抑瘤效果优于剂量更高的ARM混悬液剂型。