Inhibition of tumor angiogenesis by TTF1 from extract of herbal medicine

AIM:To study the inhibition of tumor angiogenesis by 5,2,4'-trihydroxy-6,7,5'-trimethoxyflavone(TTF1) isolated from an extract of herbal medicine Sorbaria sorbifolia.METHODS:Angiogenic activity was assayed using the chick embryo chorioallantoic membrane(CAM) method.Microvessel density(MVD) was determined by staining tissue sections immunohistochemically for CD34 using the Weidner capillary counting method.The mRNA and protein levels of vascular endothelial growth factor(VEGF),vascular endothelialgrowth factor receptor 2(VEGFR2,Flk-1/KDR),basic fibroblast growth factor(bFGF),cyclo-oxygenase(COX)-2 and hypoxia-inducible factor(HIF)-1α were detected by quantitative real-time polymerase chain reaction and Western blotting analysis.RESULTS:The TTF1 inhibition rates for CAM were 30.8%,38.2% and 47.5% with treatment concentrations of 25,50 and 100 μg/embryo × 5 d,respectively.The inhibitory rates for tumor size were 43.8%,49.4% and 59.6% at TTF1 treatment concentrations of 5,10,and 20 μmol/kg,respectively.The average MVD was 14.2,11.2 and 8.5 at treatment concentrations of 5 μmol/kg,10 μmol/kg and 20 μmol/kg TTF1,respectively.The mRNA and protein levels of VEGF,KDR,bFGF,COX-2 and HIF-1α in mice treated with TTF1 were significantly decreased.CONCLUSION:TTF1 can inhibit tumor angiogenesis,and the mechanism may be associated with the down-regulation of VEGF,KDR,bFGF,HIF-1α and COX-2.

Preliminary Validation of Tumor Cell Attachment Inhibition Assay for Developmental Toxicants With Mouse S180 Cells

This study was designed to explore the possibility of using ascitic mouse sarcoma cell line (S180) to validate the mouse tumor cell attachment assay for developmental toxicants, and to test the inhibitory effects of various developmental toxicants. The results showed that 2 of 3 developmental toxicants under consideration, sodium pentobarbital and ethanol, significantly inhibited S180cells attachment to Concanavalin A-coaed surfaces. Inhibition was dependent on concentration, and the IC50 (the concentration tha reduced attachment by 50% ), of these 2 chemicals was 1.2×10-3mol/L and 1 .0 mol/L, respectively. Anoher developmental toxiant, hydmiortisone, did not show inhibitory activity. Two non-developmental toxicants, sodium chloride and glycine were also tested and these did not decrease attachment rates. The main results reported here were generally sindlar to those obtained with ascitic mouse ovdrian tumor cells as a model. Therefore, this study added further evidence to the conclusion that cell specificity does not lindt attachment inhibition to Con A-coated surfaces, so S180 cell may serve as an altemative cell model, especially when other cell lines are unavailable. Furthermore, after optimal validation, it can be suggested that an S180 cell attachment assay may be a candidate for a series of assays to detect developmental toxicants.

PD-L1 Expression and Tumor Infiltrating Lymphocytes in Neurofibromatosis Type 1-Related Benign Tumors and Malignant Peripheral Nerve Sheath Tumors:An Implication for Immune Checkpoint Inhibition Therapy

Background Neurofibromatosis type 1(NF1)is an autosomal dominant inherited disorder.It can affect multiple systems of the body and cause severe disfigurement and discomfort in these patients.There are two types of neurofibromas,named cutaneous and plexiform neurofibromas.The latter type may transform into malignant peripheral nerve sheath tumors(MPNSTs).Surgical resection is difficult to perform owing to the complex tissue structure of neurofibromas;therefore,it is necessary to develop novel and effective therapies for the treatment of these tumors.Programmed cell death protein 1(PD-1)/programmed cell death-ligand 1(PD-L1)-related immune checkpoint inhibitors have been proven effective for various cancers,and the positive expression of PD-L1 and tumor-infiltrating lymphocytes(TILs)has been recognized as a biomarker for the response to immune checkpoint therapy.Methods We conducted immunohistochemistry(IHC)staining to detect PD-L1 expression in plexiform neurofibroma and MPNST tissue samples.Reverse transcription-polymerase chain reaction(RT-PCR)and western blotting were performed to detect PD-L1 and PD-1 expression in MPNST cell lines.IHC staining was used to show immune cell infiltration in NF1 and MPNST tissues.Results IHC staining showed PD-L1 positive expression in neurofibromas and MPNST tumor tissues.In addition,qPCR and western blotting showed high expression of PD-L1 in MPNST tumor cells.IHC staining revealed that aberrant T lymphocytes infiltrated the plexiform neurofibroma and MPNST tumor tissues.Conclusion These results indicate that immune checkpoint mechanisms may play a pivotal role in the development of NF1-related tumors,and immune checkpoint inhibitors may be effective for managing neurofibromas and MPNSTs.Combined therapy with other molecular agents may be explored in the future.

Inhibition of mouse tumors by heavy ion irradiation

Inhibition effects, control probabilities and pathology tissue changes of mouse transplanted tumors S180 after irradiation with 50 MeVu 12C6+ ions are reported. Doses of single irradiation were 0.5, 1, 2, 5, 10, 20, 40 Gy, respectivelyl at a dose rate of 3 Gy/min. Observing time was 24 days. The results show that each group had significant inhibition action on S180 tumors and all inhibitory probabilities were more than 90%; the initial time of inducing tumor inhibition effects were within one week in high dose groups （20, 40 Gy）, and after two weeks in medium dose groups （5, 10 Gy） and low dose groups （0.5, 1, 2 Gy）; also, inhibitory effects in high dose groups were obviously greater than other groups （p <0.05）; tumor control probabilities were different in each group) those in high dose groups （20, 40 Gy） were higher and TCD50 （50% tumor control dose） was 20Gy; the results for curing tumors are different in different doses; pathology inspection presented here were tumor tissue necrosis and degeneration in each dose group and they depended on doses.

Tumor microenvironment-activatable neuropeptide-drug conjugates enhanced tumor penetration and inhibition via multiple delivery pathways and calcium deposition

Peptide-drug conjugates have achieved considerable development and application as a novel strategy for targeted delivery of anticancer drugs. Bioactive peptides induced calcium deposition can irreversibly assist inhibition of tumors. However, active regulation of calcium level through signal transduction of bioactive substances has not been reported yet. In this study, novel neuropeptide-doxorubicin conjugates(NP-DOX) with lysosome-specific acid response were described for neuropeptide Y_1 receptor(Y_1R)-overexpressed triple-negative breast cancer. The delivery mechanism of NP-DOX was clarified that diverse pathways were involved, including intracellular and intercellular transport. Importantly, up-regulation of Y_1 R-mediated intracellular calcium level via second messenger inositol triphosphate was presented in NP-DOX treated MDA-MB-231 cells. In vivo antitumor efficacy demonstrated that NP-DOX showed less organ toxicity and enhanced tumor inhibition benefited from its controlled release and Y_1R-mediated calcium deposition, compared with free DOX. This bioconjugate is a proof-of-concept confirming that neuropeptide-mediated control of signaling responses in neuropeptide-drug conjugates enables great potential for further applications in tumor chemotherapy.

A proton-catalyzing prodrug for PDT and glycolysis inhibition-synergistic therapy of tumor in spatiotemporal dimensions

The reactive oxygen species(ROS)generation from photosensitizer in photodynamic therapy(PDT)is limited by tumor hypoxia.Even type-I photosensitizers,e.g.,sulfur-substituted Nile blue,still rely on oxygen as the main center for transferring electrons to generate ROS.Cutting off the pathway of oxygen consumption in tumor can help photosensitizers overcome the limitation of low oxygen,in order to efficiently generate more ROS.It is known that glycolysis inhibitor 3-bromopyruvic acid(3-BP),which could specially target mitochondria,can provide more oxygen by inhibiting oxidative phosphorylation.Herein,we successfully designed and synthesized a new 3-BP-coupled sulfur-substituted Nile blue as prodrug(NBBP)for chemical/photodynamic synergistic therapy.Major results indicated that the protons in tumor catalyzed the hydrolysis of NBBP,inhibited photoinduced electron transfer between 3-BP and the photosensitizer in NBBP and further assisted the photosensitizer to be localized in mitochondria,utilizing local oxygen as much as possible and kill tumor cells more efficiently.Moreover,the glycolysis inhibition-induced autophagy was combined with PDT-induced autophagy,which could promote the deaths of tumor cells.Unlike other remedies exploiting nanomaterials,this construction method of NBBP achieves the efficient synergy of photodynamic therapy and glycolysis inhibition,stronger than their theoretical addition,in spatiotemporal dimensions.Our study provides not only a highly efficient platform for tumor therapy but also a design approach for prodrugs with synergistic effects.

Trojan horses in tumor:engineered pyroelectric and photodynamic nanocomposites for NIR-induced cell apoptosis and tumor growth inhibition

It is desirable but always challenging to develop a cutting-edge tumor treatment strategy with high therapeutic efficacy,lesiontargeted precision and mild accessibility.Compared to traditional treatment modalities,photodynamic therapy has been widely studied since the generation of reactive oxygen species(ROS)at cancerous lesions unprecedentedly offers a convenient approach for localized tumor eliminations.Nevertheless,the consumption of oxygen for ROS production in a hypoxic tumor microenvironment has dramatically limited its feasibility and efficacy.Herein,the engineered nanocomposites of BTO@PDA-ICGHA with photodynamic and pyroelectric performances have been fabricated and applied to the photodynamic-pyroelectric dynamic treatments.The continuing ROS production derived from intracellular oxygen(O_(2))and water(H_(2)O)by laser irradiation contributed to the superb tumor cell apoptosis and significant tumor growth inhibition.Thus,this study has validated a new concept by depositing the engineered nanocomposites at the tumor just like Trojan horses,facilitating ROS release as killers and exerting the NIR-induced cell apoptosis and tumor growth inhibition with high therapeutic efficiency and expectable translational perspectives.

Treatment of gastrointestinal neuroendocrine tumors with inhibitors of growth factor receptors and their signaling pathways: Recent advances and future perspectives

The limited efficacy of conventional cytotoxic treatment regimes for advanced gastrointestinal neuroendocrine cancers emphasizes the need for novel and more effective medical treatment options. Recent findings on the specific biological features of this family of neoplasms has led to the development of new targeted therapies, which take into account the high vascularization and abundant expression of specific growth factors and cognate tyrosine kinase receptors. This review will briefly summarize the status and future perspectives of antiangiogenic, mTOR- or growth factor receptor-based pharmacological approaches for the innovative treatment of gastrointestinal neuroendocrine tumors. In view of the multitude of novel targeted approaches, the rationale for innovative combination therapies, i.e. combining growth factor (receptor)-targeting agents with chemo- or biotherapeutics or with other novel anticancer drugs such as HDAC or proteasome inhibitors will be taken into account.

Dicranostigma leptopodum (maxim) fedde induced apoptosis in SMMC-7721 human hepatoma cells and inhibited tumor growth in mice

Dicranostigma Leptopodum (Maxim) Fedde (DL- F), which had been previously documented to suppress oxidative hemolysis of erythrocytes and enhance immune functions of murine peri- toneal macrophages, was investigated for its effect on anti-tumor activity. Of alkaloids extracted from DLF, five have been identified with employment of chromatographic analysis. An antiproliferative role of these alkaloids was determined on SMMC-7721 Human Hepatoma Ce- lls in an apoptosis-inducing manner, through MTT assaying, Trypan blue exclusion assaying and cytometric analysis of cell cycle distribution. To further examine their inhibitory effects on tumor progression, murine H22 cells were inoculated into Kunming mice to determine the role of these alkaloids of DLF in inhibiting tumor growth in the tumor-implanted mice. It was found that these alkaloids of DLF enhanced the tumor shrinkage effectively wherein its tumor inhibitory rate and immunohistochemistry stain- ing of the tumor were determined and profiled, respectively.

Synthesis of Fluorinated Heterobicyclic Nitrogen Systems Containing 1,2,4-Triazine Moiety as CDK2 Inhibition Agents

New fluorine substituted heterobicyclic nitrogen system as imidozolopyrimidines (2,3), pyrimido- 1,2,4-triazinones (4-7), 1,2,4-triazinyl-1,2,4-triazine (12-16), 1,2,4-triazinyl-1,2,4-triazinones (14-17) and substituted thiobarbituric acids (19-20), have been synthesized using the reaction of 3- amino-5,6-di (4'-fluorophenyl)-1,2,4-triazine (1) with α,β–bifunctional compounds. Structures of the title compounds were characterized by UV, IR, 1H/13C-NMR and mass spectrometric method. The studied compounds were tested for CDK2 inhibiting activity in DNA damage, as well as in vitro anti-tumor activity.

鳖甲煎丸对肝癌大鼠黏着斑激酶/雷帕霉素靶蛋白通路的影响

目的:探讨鳖甲煎丸对肝癌模型大鼠肝组织病理特征及FAK/mTORC1通路的影响。方法:HepG2(1×10^(7))细胞注射于大鼠右腋皮下,建立肝癌模型,分为模型组、5-氟尿嘧啶组、鳖甲煎丸低剂量组、鳖甲煎丸高剂量组,另设正常组。各药物组给予相应药物灌胃,持续给药4周,正常组、模型组给予等体积的0.9%氯化钠溶液。实验结束后,测定肝癌组织重量、肝癌组织体积、肝癌组织抑瘤率、肝癌FAK、mTORC1水平、肝癌VEGFR-2、VEGF、IL-4、IL-8、TNF-α蛋白水平。结果:与正常组比较,模型组肝癌组织重量、肝癌组织体积、肝癌组织抑瘤率、VEGFR-2、VEGF、IL-4、IL-8、TNF-α蛋白、肝癌FAK、mTORC1 mRNA和蛋白表达升高(均P<0.05)。与模型组比较,5-氟尿嘧啶组、鳖甲煎丸低剂量组、鳖甲煎丸高剂量组肝癌组织重量、肝癌组织体积、肝癌组织抑瘤率、VEGFR-2、VEGF、IL-4、IL-8、TNF-α蛋白、肝癌FAK、mTORC1 mRNA和蛋白表达降低(均P<0.05)。鳖甲煎丸高剂量组肝癌组织重量、肝癌组织体积、肝癌组织抑瘤率、VEGFR-2、VEGF、IL-4、IL-8、TNF-α蛋白、肝癌FAK、mTORC1 mRNA和蛋白表达低于鳖甲煎丸低剂量组(均P<0.05)。结论:鳖甲煎丸对大鼠肝癌具有明显抑制作用,能减轻大鼠肝癌所致的病理损伤,其机制可能与鳖甲煎丸抑制肝癌FAK、mTORC1表达,诱导肝癌细胞凋亡,降低炎症反应有关。

长链非编码RNA GC1靶向微小RNA-551b-3p抑制食管癌的作用及分子机制研究

目的探讨长链非编码RNA(LncRNA)鸟苷酸环化酶1(GC1)对食管癌的影响,并探讨其靶向微小RNA-551b-3p(miR-551b-3p)的分子机制。方法建立食管癌荷瘤裸小鼠模型,随机分为GC1、miR-551b-3p上、下调组及其对应对照组与模型组共9组,每组8只。末次给药次日处死裸小鼠,称取瘤体质量,计算抑瘤率;取肿瘤组织检测LncRNA GC1、miR-551b-3p基因表达水平和细胞周期因子(CyclinD1)、p21、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关x(Bax)基因与蛋白表达水平;观察肿瘤组织病理改变;采用流式细胞术检测肿瘤细胞凋亡率;采用双荧光素酶报告基因实验验证LncRNA GC1与miR-551b-3p的调控关系。另取人食管癌细胞株Eca109分为9组,每组3个复孔,其中基因干扰组命名同上,另设置空白组,培养48h后观察细胞LncRNA GC1、miR-551b-3p基因表达水平、形态学改变、凋亡率、CyclinD1、p21、Bcl-2、Bax基因与蛋白表达水平。结果动物实验:与模型组和相应对照组比较,GC1上调组与miR-551b-3p下调组瘤体质量、CyclinD1和Bcl-2基因与蛋白表达水平均上升,抑瘤率、细胞凋亡率、miR-551b-3p基因、p21和Bax基因与蛋白表达水平均下降;GC1下调组与miR-551b-3p上调组瘤体质量、CyclinD1和Bcl-2基因与蛋白表达水平均下降,抑瘤率和细胞凋亡率、miR-551b-3p基因、p21和Bax基因与蛋白表达水平均上升;GC1上调组LncRNA GC1基因表达水平上升,GC1下调组LncRNA GC1基因表达水平下降(P<0.05)。与转染野生型GC1的腺病毒载体相比,转染突变型GC1的腺病毒载体的miR-551b-3p荧光素酶相对活性上升(P<0.05)。细胞实验:LncRNA GC1和miR-551b-3p基因表达水平、细胞形态学改变与凋亡率、CyclinD1、p21、Bcl-2、Bax基因与蛋白表达水平变化趋势均与动物实验相同。结论下调LncRNA GC1、上调miR-551b-3p表达水平均可抑制食管癌进展,且下调LncRNA GC1可靶向上调miR-551b-3p,并降低CyclinD1和Bcl-2活性、上升p21和Bax活性。

抗肿瘤药效研究中疗效与安全性综合评价指标的选择

目的传统抗肿瘤药效评价指标中体质量、肿瘤体积和抑瘤率可以分别体现制剂的安全性和疗效,但是单一指标并不能兼顾这两点。为此,新的抗肿瘤药效评价指标被提出,其中抑瘤指数可以全面地呈现药物的治疗效果。方法以表柔比星相关制剂的药效学实验数据为例,对“新”和“旧”抗肿瘤评价指标的统计结果进行分析。结果聚乙二醇修饰脂质体组内小鼠的抑瘤率(0.80±0.05)与唾液酸修饰脂质体组内小鼠的抑瘤率(0.89±0.01)无显著性差异(P≥0.05),但是聚乙二醇修饰脂质体组内小鼠的抑瘤指数(40±9)显著低于唾液酸修饰脂质体组内小鼠的抑瘤指数(82±7,P<0.001)。结论“新”抗肿瘤评价指标更适合用于抗肿瘤研究的数据分析。

幽门螺杆菌感染对胃黏膜上皮细胞病变的研究进展

通过系统阐述幽门螺杆菌在不同机制下通过诱导通路活性与胃黏膜上皮细胞病变的联系,从而探讨延缓胃黏膜上皮细胞恶性病变的新方法。通过对比胃黏膜上皮细胞病变过程中影响通路的不同发病机制,从而研究影响胃黏膜上皮细胞恶性病变的相关活性通路。大量研究证明,幽门螺杆菌感染通过细胞毒素相关基因A(CagA)依赖性和非依赖性机制引发诱导不同通路发挥作用。同时,在CagA依赖/非依赖性作用条件下,幽门螺杆菌可以通过作用于p53肿瘤抑制因子,从而促进胃黏膜上皮细胞发生恶变,是胃癌的重要致病原因之一。通过对胃黏膜上皮细胞与幽门螺杆菌相关作用的深入研究,找出延缓胃黏膜病变进展的作用机制,为临床上治疗幽门螺杆菌感染所致的一系列胃肠道疾病提供新思路。

常山酮和盐霉素协同抑制犬乳腺肿瘤细胞的增殖、迁移和克隆形成

旨在以犬乳腺肿瘤组织上分离所得的细胞CMT-N7为体外模型,评估常山酮和盐霉素联用对犬乳腺肿瘤细胞增殖、迁移和克隆形成的影响。采用常山酮、盐霉素单独以及两药联合处理,评估对犬乳腺肿瘤细胞的抑制作用,使用Chou-Talalay方法计算联合指数,确定最佳协同比例,进一步使用划痕试验和克隆形成试验评估两药在协同比例下联用对犬乳腺肿瘤细胞迁移和克隆形成能力的影响。结果显示:常山酮和盐霉素呈浓度依赖性地抑制CMT-N7细胞的增殖,且两药联用具有协同抑制作用,最佳协同比例为1∶1,该比例下两药联用对犬乳腺肿瘤细胞的迁移和克隆形成的抑制作用比单药更显著(P<0.01)。因此,常山酮和盐霉素联用能够协同抑制犬乳腺肿瘤细胞的增殖、迁移和克隆形成。本研究为兽医临床抗肿瘤药物的联合应用提供了依据。

灰树花醇提物化学成分及其生物活性研究

为探明灰树花发挥活性作用的化学成分及其抗氧化活性和对肿瘤细胞的抑制作用,该文分析了灰树花醇提物不同极性溶剂萃取物的主要化学成分及其对1,1-二苯基-2-三硝基苯肼(DPPH)自由基、2,2’-联氮-双-3-乙基苯并噻唑啉-6-磺酸(ABTS)自由基和羟自由基的清除能力,以及对肝癌细胞(HepG2)和肺癌细胞(A549)的抑制作用。结果显示,乙酸乙酯萃取物和正丁醇萃取物的抗氧化活性最佳,总酚和黄酮的质量分数与抗氧化活性显著正相关(P<0.05);石油醚萃取物和乙酸乙酯萃取物对肿瘤细胞抑制效果最好,三萜和甾醇质量分数与肿瘤细胞抑制作用极显著正相关(P<0.01)。利用超高效液相色谱质谱联用技术(UPLC-MS)从灰树花醇提物中共鉴定出15个化合物,其中芹菜素和表儿茶素可能是灰树花发挥抗氧化作用的主要化学成分,麦角甾醇和过氧化麦角甾醇可能是发挥肿瘤细胞抑制作用的甾体类化合物。该研究结果可为灰树花作为功能食品进一步开发提供理论依据。

肿瘤抑制蛋白PDCD4结构特性与疾病关系解析及研究进展

程序性细胞死亡蛋白PDCD4(programmed cell death 4)是一种肿瘤抑制蛋白,在多种肿瘤组织中下调并提示不良预后,是第一种被发现通过抑制翻译抵抗肿瘤转化、侵袭和转移的蛋白质。PDCD4自身结构与功能关系密切,并受细胞外信号影响,其蛋白表达水平和功能与人体两大信号通路PI3K-Akt-mTOR和MAPK密切相关,通过多种机制调节与肿瘤相关的其他蛋白质。本文通过解析PDCD4结构、功能与疾病的关系,总结了近年来PDCD4在凋亡、自噬、肿瘤、炎症等生理过程和疾病中的作用,为PDCD4及相关蛋白的信号传导路径研究和以它们为靶标的疾病治疗提供启发和思路。

细菌与肿瘤的关系

人体携带有数以万亿计的细菌,其中大部分细菌与人体之间已经形成互惠互利的共生关系。细菌群落失调或者病原细菌感染会通过炎症以及分泌代谢物对人类健康产生负面影响,从而导致各种疾病的发生,这其中也包括肿瘤。细菌可以影响人体内肿瘤的发生发展,一方面细菌可以通过诱导慢性炎症、引起DNA损伤、激活核心致瘤信号通路等机制促进肿瘤的发生;另一方面又可以通过自身的溶瘤作用或者激活适应性免疫细胞来抑制肿瘤生长,此外通过基因工程修饰,一些被设计成低毒高效的药物输送的细菌已经成功地用在动物模型或临床试验中的肿瘤治疗。该文从细菌是如何促进肿瘤和肿瘤治疗上的应用两个方面综述近期有关细菌和肿瘤发生发展的相关文献,以期为肿瘤的治疗提供一种新的治疗思路。

聚乙二醇修饰的树状大分子负载卡巴他赛的制备工艺优化及抗肿瘤活性研究

目的 制备一种高效递送卡巴他赛(CTX)的聚乙二醇(PEG)修饰树状大分子递送胶束(mPEG-PAMAM),优化处方和制备工艺。方法 聚酰胺-胺树状大分子(PAMAM)与PEG发生迈克尔加成反应得到mPEG-PAMAM胶束,经纳米沉淀法进行药物装载,通过红外光谱、核磁共振氢谱鉴定合成材料的结构;通过透射电镜和激光粒度仪观察载药胶束的外貌形态并测定其粒径、电位;高效液相色谱法测定其载药量、包封率等;通过MTT等实验考察其细胞毒性,共聚焦显微镜探究其细胞摄取情况;在动物水平上注射RM-1前列腺癌细胞构建小鼠肿瘤模型,探究其整体抑瘤能力。结果 mPEG-PAMAM@CTX胶束呈较规则的球形,平均粒径(162.8±0.7)nm,载药量6.58%,包封率61.12%,48 h内药物累计释放量达到86.8%;mPEG-PAMAM@CTX具有良好的细胞摄取,能有效地杀伤肿瘤细胞;在体内动物模型中,CTX经体内循环,主要富集在肿瘤部位,表明CTX能够通过mPEG-PAMAM胶束高效递送到RM-1肿瘤组织,且肿瘤抑制率为68.97%。结论 本研究制备的mPEG-PAMAM@CTX胶束能够有效提高CTX溶解度,增强肿瘤抑制效果,为难溶性药物递送的开发提供新的思路。