The ralationship between fractional anisotropy value and tumor microarchitecture in late-stage rat glioma

Objective: To explore the magnetic resonance diffusion tensor imaging(MR-DTI) features of in the late stage of Wistar rat C6 brain glioma, and the relationship between fractional anisotropy value and tumor microarchitecture. Methods: The concentration of more than 1.0×伊 106/10 μL glioma cells and complete medium were injected stereotactically into the right caudate nucleus of the experimental group(n=35) and control group(n=10), respectively. Conventional MRI, DTI, and enhanced T1 WI scans were Performed using the GE Signa HD× 3.0T MRI scanner about 3-4 weeks after implantation for the rats. Postproeessing was done using the DTI specific software Function Tool to gain FA image. Many ROIs were drawn avoiding hemorrhage, necrosis areas in tumor parenchyma, the value of FA was recorded. Each surviving rat brain was examined histologically using HE and immunohistochemical staining for VEGF and CD34. Pearson correlation analysis was used to determine the relationships between FA values and VEGF, MVD, cell density, respectively. Results: A total of 35 tumor-bearing rats were confirmed the tumor formation by the subsequent MRI and pathological examination. The mean FA values of the tumor and the contralateral brain tissue were 0.17 ± 0.03 and 0.31 ± 0.05 respectively, and the difference was statistically significant(t = 12.80, P <0.05). The mean FA value of grade III glioma(n=12) was 0.16 ± 0.03, and the average FA value of grade IV glioma(n=23) was about 0.18 ± 0.04. There was no significant difference between the two groups(t= 1.92, P> 0.05). FA value in the late stage of Wistar rat C6 brain glioma has significant positive correlation to VEGF, MVD, cell density. The correlation coefficients between FA and VEGF, MVD, and cell density were 0.67, 0.65 and 0.71(P<0.05), respectively. Conclusions: The FA value of rat glioma tumor in the late stage can preoperatively provide an accurate, reliable and noninvasive imaging monitoring method to evaluate the microstructure of glioma( cell density, the extent of angiogenesis, fiber bundle integrity and tumor cell infiltration and so on), predict the biological behavior of the tumor and make out surgical plan.

The 9L^(LUC)/Wistar rat glioma model is not suitable for immunotherapy

The availability of a well-characterized animal brain tumor model will play an important role in identifying treatments for human brain tumors. Wistar rats bearing 9L glioma cells can develop solid, well-circumcised tumors, and may be a useful animal model for the evaluation of various therapeutic approaches for gliosarcomas. In this study, the 9L/Wistar rat glioma model was produced by intracerebral implantation of 9L^LUC glioma cells syngenic to Fischer 344 （F344） rats. Bioluminescence imaging showed that tumors progressively grew from day 7 to day 21 in 9L^LUC/F344 rats, and tumor regression was found in some 9L^LUC/Wistar rats. Hematoxylin-eosin staining verified that intracranial tumors were gliomas. Immunohistochemistry results demonstrated that no CD4- and CD8-positive cells were found in the syngeneic 9L^LUC/F344 model. However, many infiltrating CD4- and CD8-positive cells were observed within the tumors of the 9L^LUC/Wistar model. Our data suggests that compared with 9L/F344 rats, 9L glioma Wistar rats may not be suitable for evaluating brain glioma immunotherapies, even though the model induced an immune response and exhibited tumor regression.

Heat shock induction of a 65 kDa ATP-binding proteinase in rat C6 glioma cells

The 45, 55, 65 and 100 kDa ATP-binding proteinases (ATP-BPases) of the heat-shocked (44 ℃ for 30 min, recovery for 12h) rat C6 glioma cells were purified by DEAE-ionexchange and ATP-affinity chromatography. Their molecular masses, isoelectric points (pI), pH-optima and other properties were analyzed by native proteinase gels.It was shown that the 65 kDa ATP-BPase is specifically induced by heat shock and not detectable in control cells.Its N-terminal 1-9 amino acid sequence was determined by Edman degradation, but no homologies to other proteins in the protein data bases were found. 30 and 31 kDa proteinases can be cleaved from the 45, 55 and 65 kDa proteinases to which they are linked. A possible relationship of the heat-induced 65 kDa ATP-BPase with the ATP-dependent proteinases (ATP-DPases) in prokaryotes and eukaryotes is discussed.

Bone marrow stromal cell versus neural stem cell transplantation in a C6 glioma rat model

BACKGROUND： Embryonic neural stem cells （NSCs） have provided positive effects for the treatment of glioma. However, the source for embryonic NSCs remains limited and high amplification conditions are required. Bone marrow stromal cells （BMSCs） have been proposed for the treatment of glioma. OBJECTIVE： To investigate biological changes in NSCs and BMSCs following transplantation into rat models of glioma. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Embryonic Stem Cell Research Laboratory of Yunyang Medical College from February 2006 to August 2008. MATERIALS： The rat C6 glioma cell line was purchased from Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences; mouse anti-bromodeoxyuridine （BrdU） monoclonal antibody and Cy3-1abeled goat anti-mouse IgG antibody was purchased from Upstate, USA. METHODS： A total of 95 Sprag6ue Dawley rats were randomly assigned to three groups： NSC （n = 35）, transplanted with 〉 6 × 10^6 NSCs via left medial hind limb; BMSC （n = 35）, transplanted with 〉 1 × 10^6 BMSCs via left medial hind limb; model group （n = 25）, injected with the same volume of 0.1 mmol/L phosphate buffered saline. MAIN OUTCOME MEASURES： Gliomal growth and size were assessed by nuclear magnetic resonance, and glioma morphological features were observed following hematoxylin-eosin staining and BrdU immunohistochemistry 3 and 4 weeks following transplantation. RESULTS： The average survival of rats in the BMSC, NSC, and model groups was 4.03, 4.28, and 3.88 weeks. At 3 weeks, there was no significant difference in the average glioma diameter between the BMSC and model groups （P 〉 0.05）. However, gliomal diameter was significantly decreased in the NSC group compared with the model group （P 〈 0.05）. At 4 weeks, there was no statistical difference between the groups （P 〉 0.05）. BrdU immunohistochemistry revealed that BMSCs and NSCs appeared to migrate to the gliomas. CONCLUSION： NSCs inhibited glioma cell growth and prolonged rat survival. BMSCs did not significantly suppress glioma cell growth.

An experimental study on N-ethyl-N-nitrosourea-induced rat brain gliomas

Rat brain gliomas were induced by transplacental and subcutaneous administration of synthesized Nethyl-N-nitrosourea(EVU, 60 mg/kg body weight) in the late gestational and 3-day Wistar rats respectively, observed until the end of 12th month after administration.The incidences of tumor formation were 73. 2% and 68.3% (those of gliomas were 65. 9% and 63. 4%) respectively. Histologically, the main types were mixed oligodendro-astrocytomas and oligodendrogliomas, with the characteristics of being microfocal, multifocal and mixed, in presence with focal and/or diffuse proliferation of glial cells. The results showed that these glioma models induced by the synthesized ENU were successful and stable, serving a fine approach to further study of the initiation,growth and differentiation of gliomas. The significance of proliferation of glioblasts in the oncogenesis of ENU-induced gliomas was discussed in this report.

Inhibitory effects of Pseudomonas aeruginosa mannose-sensitive hemagglutinin on rat C6 glioma cell proliferation

BACKGROUND： Pseudomonas aeruginosa mannose-sensitive hemagglutinin （PA-MSHA） parenteral injection is used as a broad-spectrum immunomodulator. It remains unclear whether PA-MSHA exhibits inhibitory effects on tumor cell growth. OBJECTIVE： To investigate inhibitory mechanisms of PA-MSHA-induced proliferation in rat C6 glioma cells in vitro. DESIGN, TIME AND SETTING： Comparative observation and in vitro experiments were performed at the Key Laboratory of Natural Medicine, Kunming Medical College, China from July 2008 to April 2009. MATERIALS： Rat C6 glioma cell line （Shanghai Institute of Cell Biology, Chinese Academy of Sciences, China） and PA-MSHA parenteral injection （Beijing Wanteer Bio-Pharmaceutical, China） were used in the present study. METHODS： Rat C6 glioma cells in logarithmic growth phase were harvested in vitro. Adherent monolayer cells were respectively treated with PA-MSHA at final colony-forming units （cfu） of 1 ×10^8 cfu/mL, 2 × 10^8 cfu/mL, 4 × 10^8 cfu/mL, 6 × 10^8 cfu/mL, and 8 ×10^8 cfu/mL following 24 hours of conventional culture. MAIN OUTCOME MEASURES： MTT colorimetric assay was utilized to determine the inhibitory rate of C6 glioma cells following treatment with various concentrations of PA-MSHA at different times. Cell apoptosis was detected by fluorescent microscopy following Hoechst 33258 staining. Flow cytometry was used to measure PA-MSHA effects on C6 cell cycle. RESULTS： Inhibitory rate of C6 glioma cells increased with prolonged time and increased dose. Hoechst 33258 staining revealed obvious morphological changes in apoptotic C6 glioma cells. Flow cytometry revealed hypodiploid peaks, Le., apoptotic peak, and the apoptotic rate in cells during S-phase significantly increased with increased concentrations in the experimental groups. CONCLUSION： With in vitro experiments, PA-MSHA preparations inhibited C6 glioma cell proliferation in a time- and dose-dependent manner. These mechanisms are likely associated with cell apoptosis induction and inhibition of the S phase.

EXPERIMENTAL STUDY ON THE GENE THERAPY OF MALIGNANT GLIOMA WITH ANTISENSE VEGF RNA

Objective: To study the effect of antisense VEGF RNA on rat C6 gliomas in vivo and find out the feasibility ofantiangiogenesis therapy with antisense VEGF RNA formalignant gliomas. Methods: Parental rat C6 glioma cells and C6 cells transfected with antisense VEGF cDNA were implanted intracerebrally and subcutaneously into SD rats as control and transfected group. Rats bearing cerebral and subcutaneous C6 gliomas were treated with antisenseVEGF cDNA as treated group and sense VEGF cDNA and empty vector as control of treated group. The generalmanifestation, survival time, MRI and histopathologicalchanges of all rats were observed. The volume ofsubcutaneously implanted tumors was determinedregularly. In situ hybridization and immunohistochemicalstaining were used for detection of VEGF gene expression of gliomas while PCNA immunostaining and TUNELmethod for examination of proliferation activity andapoptosis of gliomas, respectively. Results: The survival of the rats in transfected and treated group was prolonged.There were two rats surviving over 90 d in the treatedgroup and their tumors disappeared. The VEGF geneexpression, the number of microvessels and theproliferation activity were decreased and a large amount of apoptotic cells could be found in cerebral and subcutaneous gliomas in treated and transfected groups. Conclusion:VEGF is one of the candidate genes for gene therapy ofmalignant gliomas. Antisense VEGF RNA combined with other therapies should be studied further for enhancing the therapeutic effect of malignant gliomas.

IN VIVO GROWTH OF CEREBRAL C6 GLIOMA CELLS TRANSFECTED AND TREATED WITH CX43 GENE

Objective: To study the role of connexin gene (Cx 43) on the development of glioma and the feasibility of using Cx43cDNA as a target of gene therapy of gliomas. Methods: Parental rat C6 cells and C6 cells transfected with Cx43cDNA were implanted into right caudate nucleus of SD rats as control and transfected group. Rats bearing cerebral C6 gliomas were treated with Cx43cDNA and empty vector as treated group and empty vector group. The general manifestation, survival time, MRI dynamic scanning and histopathological changes of all rats were observed. In situ hybridization and immunohisto- chemistry were used for examination of Cx43mRNA and its protein in gliomas. Average number of AgNOR staining was used for detection of cell proliferation activity, and TUNEL method for determination of cell apoptosis. Results: All rats in control and empty vector group died of cerebral gliomas within 3 weeks after implantation of C6 cells. Six out of nine rats in the transfected group and eight out of ten rats in treated group kept alive beyond 120 days with totally disappearing of the tumor foci, except one treated rat having a little residue of tumor. In gliomas of transfected and treated groups Cx43 gene expression was upregulated, proliferation activity was lowered, However, the apoptotic cells did not increase. Conclusion: The present study indicates that Cx43 gene is of crucial importance in the development of malignant glioma. It can be an effective target for gene therapy of gliomas.

悬浮法培养C6胶质瘤细胞系和该细胞系中脑肿瘤干细胞的分离

目的研究应用无血清培养基悬浮法培养C6胶质瘤细胞系的方法;并分离该细胞系中的脑肿瘤干细胞,观察其生长方式和分化特征。方法应用培养大鼠神经干细胞的培养基和培养方法,在无血清培养基中采用悬浮法培养大鼠C6胶质瘤细胞系;再将分离获得的悬浮生长的脑肿瘤干细胞接种于含血清培养基,观察其分化;应用有限稀释和单克隆形成实验确定该细胞系中肿瘤干细胞的比例。结果C6胶质瘤细胞系中有约1.18%的肿瘤细胞在无血清培养基中能够存活、增殖,形成自由漂浮的细胞球;这种细胞球具有人脑肿瘤干细胞球的特征,并可连续传代,若重新接种于含血清培养基中可重新贴壁分化,贴壁分化后细胞形态与直接在含血清培养基中培养的C6胶质瘤细胞系无明显差别。结论C6大鼠胶质瘤细胞系中含有比例较低的、具有增殖和分化能力脑肿瘤干细胞(约1.18%),该细胞系可在含生长因子的无血清培养基中悬浮生长,并维持细胞系。

大鼠C6脑胶质瘤CT灌注成像的初步研究

目的初步探讨CT灌注成像技术用于大鼠C6脑胶质瘤微循环研究的可行性。方法采用立体定向方法在20只雌性Wistar大鼠右侧尾状核接种C6细胞,荷瘤大鼠分为二组,一组于接种后1、2、3周分别行MR检查以评价肿瘤生长,另一组于接种后2周时行CT灌注成像,每次检查结束后留取鼠脑标本作病理学检查。结果大鼠C6脑胶质瘤的生长特征及MR表现符合文献报道。肿瘤区脑血流量(CBF)、脑血容量(CBV)、对比剂平均通过时间(MTT)和表面通透性(PS)及瘤脑交界处CBV,MTT,PS值均明显大于对侧正常脑组织(P<0.05),肿瘤中心PS值大于肿瘤周边(P<0.05),CBF、CBV、MTT则无统计学差异(P>0.05);肿瘤区有较多新生血管,肿瘤周边更为丰富。结论CT灌注成像可用于研究大鼠C6脑胶质瘤的微循环变化。

骨髓间充质干细胞与胶质瘤细胞非接触共培养后相关生物学特性分析

目的在体外通过大鼠胶质瘤C6细胞与大鼠骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)非接触共培养,以探明BMSCs是否受到肿瘤微环境的作用获得肿瘤细胞的相关生物学特性。方法通过6孔板结合Transwell小室建立BMSCs和C6胶质瘤细胞的共培养体系,以共培养组为实验组,设单独培养的BMSCs为对照组;相差显微镜下观察培养后2组细胞形态学的改变;核干细胞因子(nucleostemin,NS)检测细胞增殖力的变化;荧光定量PCR和Western blot检测细胞中mdm2、p53mRNA水平及其蛋白的变化;免疫荧光法检测神经胶质细胞特异的胶质纤维酸蛋白(glial fibrillary acidic protein,GFAP)在细胞中的定位及表达。结果共培养后实验组细胞呈现类似胶质瘤细胞样的形态,表达神经胶质细胞特异的GFAP蛋白;NS蛋白反映的细胞增殖能力未发生改变;共培养后实验组p53mRNA水平明显低于对照组(P<0.01),而p53蛋白的表达水平显著高于对照组[(1.63±0.31)vs(0.85±0.12),P<0.05];实验组mdm2mRNA及其蛋白的表达水平均明显高于对照组(P<0.05)。结论肿瘤微环境可能会使大鼠骨髓间充质干细胞获得肿瘤细胞的相关生物学特性。

大鼠C6脑胶质瘤动物实验模型的建立

目的 为脑胶质瘤的基础理论、临床治疗和药效学研究提供简便、经济、实用的大鼠C6脑胶质瘤动物实验模型。方法 采用自制大鼠脑固定架 ,固定后 ,于脑靶点接种C6胶质瘤细胞。观察动物行为状态和生存期 ,并对脑肿瘤进行形态学 ,细胞学和分子生物学相关指标的检测。结果 接种C6胶质瘤细胞后 ,动物进食量减少 ,体重下降 ,有的动物出现眶周出血 ,眼球突出 ,自身旋转 ,癫痫发作 ,偏瘫等症状 ,大约在 2至 3周内 ,动物大多死亡 ,病理解剖显示颅内肿瘤形成。结论 该方法建立的脑胶质瘤具有与人脑胶质瘤相似的特性 ,肿瘤形成时间短 ,存活期较稳定 ,可供脑胶质瘤基础理论、实验治疗和药效学研究的需要。

9L/F344大鼠脑胶质瘤模型的建立

目的建立稳定的9L/F344大鼠脑胶质瘤模型。方法15只近交系雄性F344大鼠,采用立体定向技术,在大鼠右侧额叶尾状核接种1×105个9L细胞,观察大鼠生存状态;接种后第10、20天行MRI检查,观测颅内肿瘤生长情况。大鼠死亡后,取脑制作病理切片,行HE染色后观察肿瘤组织形态,采用免疫组织化学方法检测胶质纤维酸性蛋白(GFAP)和S-100蛋白。结果大鼠接种肿瘤细胞后30d内全部死亡,平均生存时间(24.4±3.3)d。接种后10d,MRI增强扫描即可见肿瘤生成;接种后20d,MRI检查可见接种侧脑组织大片水肿,增强扫描肿瘤显像清晰。脑内均见肿瘤形成,未见肿瘤颅外生长;肿瘤周边界线较明显,但未见包膜;瘤内新生血管丰富,可见出血、坏死;肿瘤免疫组织化学GFAP和S-100蛋白染色阴性。结论该方法建立的大鼠脑胶质瘤模型稳定可靠,符合恶性胶质肉瘤生物学特性。该模型是理想的脑胶质瘤实验研究材料。

体外柴胡皂苷元d对C_6大鼠神经胶质瘤细胞前列腺素E_2生成的影响

目的 观察柴胡皂苷元d(saikogenind ,SGD)对C6大鼠神经胶质瘤细胞体外前列腺素E2 (PGE2 )生成的影响。方法 用放射性免疫法测定细胞产生的PGE2 ,液体闪烁测量法测定14 C花生四烯酸 (AA)标记细胞释放14 C AA。结果 SGD在 1～ 2 0 μmol·L-1范围内 ,抑制由钙离子载体A2 3187诱发C6大鼠神经胶质瘤细胞前列腺素E2 (prostaglandinE2 ,PGE2 )释放 ,其IC50 为 3μmol·L-1,但对花生四烯酸 (arachi donicacid ,AA)释放无影响。SGD不影响细胞微粒体组分将AA转化为PGE2 。结论 SGD抑制由钙离子载体A2 3187诱发体外C6大鼠神经胶质瘤细胞PGE2 产生 ,但不抑制AA释放和直接抑制环氧脂酶 (cyclooxygenase ,COX)活性。

Endostatin-Angiostatin融合基因治疗大鼠C6胶质瘤的3.0T磁共振动态观察

目的探讨3.0T磁共振在重组单纯疱疹病毒介导的Endostatin-Angiostatin(Endo-Angio)融合基因对大鼠C6胶质瘤疗效评价中的作用。方法30只雄性Wistar大鼠采用立体定向方法在颅内接种C6细胞,将荷瘤大鼠随机分为两组,治疗组与对照组;两组大鼠分别于接种后1、2、3周进行MR检查;第2、3周检查结束后每组留取2只鼠脑标本进行病理学检查;治疗组大鼠于第1周检查后于肿瘤接种位置原位注入Endo-Angio融合基因进行治疗。结果第1周检查共25只大鼠成瘤(成功率83%),第2周两组肿瘤体积均增大,二者无统计学差异(P>0.01),病理检查显示治疗组大鼠微血管腔减少,间质水肿及细胞水肿较对照组明显严重;第3周时治疗组大鼠体积减小,小于对照组(P<0.01)。结论重组单纯疱疹病毒介导的Endo-Angio融合基因对大鼠C6胶质瘤的生长有抑制作用,3.0T磁共振可以较好地动态观察大鼠C6胶质瘤的生长及治疗变化。

Gd-DTPA对磁共振扩散张量成像评估晚期鼠脑胶质瘤的影响

目的探讨Gd-DTPA对3.0T磁共振扩散张量成像(diffusion tensor imaging,DTI)评估晚期鼠脑胶质瘤的影响。方法雌性Wistar大鼠35只,通过脑固定装置将C6细胞接种至右尾状核,3~4周后分别于注射对比剂钆喷替酸葡甲胺(Gd-DTPA)前后行DTI扫描,选取瘤体、瘤周组织和对侧镜像脑组织多个感兴趣区(ROI)获得FA值,采用配对t检验分析注射对比剂前后相应部位FA值差异。结果 35只晚期C6鼠脑胶质瘤进行了DTI扫描,注射对比剂Gd-DTPA后瘤体及瘤周组织FA值均较注射对比剂前FA值升高,两组差异有统计学意义(P<0.05)。而对侧镜像脑组织注射对比剂前后FA值差异无统计学意义(P>0.05)。结论静脉注射Gd-DTPA 6 min后对大鼠C6脑胶质瘤进行DTI扫描,可人为造成瘤体及瘤周组织FA值升高,而对侧镜像脑组织FA值无明显影响,因而在进行DTI扫描时,应在注射对比剂前完成。

全反式维甲酸诱导大鼠C6脑胶质瘤细胞凋亡的实验研究

目的:探讨全反式维甲酸对大鼠C6脑胶质瘤细胞的增殖抑制及其分子机制。方法:MTT法检测全反式维甲酸作用于大鼠C6脑胶质瘤细胞后,观察其对细胞增殖抑制率的影响。流式细胞仪观察肿瘤细胞周期及凋亡率的变化。电镜观察C6细胞超微结构变化。Western blot法在不同时间点对凋亡相关基因caspase-3活性蛋白产物的表达进行了检测。结果:MTT结果表明ATRA对C6细胞的抑制作用具有时间和浓度依赖性。流式细胞仪检测证明与对照组相比,处理组C6细胞发生G1期阻滞;S、G2期细胞比例下降;细胞出现亚二倍峰,凋亡比例明显增加。电镜下全反式维甲酸作用72h后处理组C6细胞呈凋亡改变:如核固缩、染色质趋边凝聚。Western blot检测发现,处理组出现了caspase-3蛋白活性裂解片段。结论:全反式维甲酸抑制C6脑胶质瘤细胞生长,全反式维甲酸抑制脑胶质瘤的作用机理可能至少通过改变细胞周期分布、诱导凋亡来实现。

Wistar大鼠C_6胶质瘤动物模型的肿瘤生长特点

目的 :探讨Wistar大鼠颅内及皮下接种C6胶质瘤细胞的肿瘤生长特点及病理特征。方法 :第一组Wistar大鼠及SD大鼠各 5 0只 ,应用立体定向方法将 10 6的C6细胞接种于大鼠脑尾状核 ,对比观察接种后不同大鼠生存时间及病理特征。第二组 140只Wistar大鼠于颅内接种后 3d、5d、7d、9d、11d、13d和 15d各处死 2 0只 ,观察肿瘤大小及病理学变化。第三组 5 0只Wistar大鼠皮下接种 2× 10 6的C6细胞 ,观察皮下肿瘤生长特点及病理特征。结果 :Wistar大鼠颅内接种后平均生存期为 (15 9± 1 2 )d ,瘤组织向正常脑组织浸润生长 ,无明显分界 ,有肿瘤血管 ,坏死 ,卒中发生 ,S 10 0及GFAP染色阳性。SD大鼠平均生存期为 (18 9± 1 8)d ,瘤组织与正常脑组织有明显分界。Wistar大鼠颅内接种后第 5～ 11d肿瘤生长最为迅速。Wistar大鼠皮下接种后肿瘤生长稳定 ,但接种后 2 5d停止生长并逐渐缩小。结论 :Wistar大鼠颅内C6胶质瘤模型特征更加接近于人恶性脑胶质瘤 。

大鼠C6脑胶质瘤的CT灌注成像研究

目的:运用CT灌注成像评价大鼠C6脑胶质瘤的生长及其血管生成。方法:采用立体定向方法在30只雌性Wistar大鼠右侧尾状核接种C6细胞,于接种后1w、2w、3w分别进行CT灌注成像,每次检查结束后留取鼠脑标本作病理学检查。结果:荷瘤1w组肿瘤区各灌注参数值均比对侧正常脑组织增大(P<0.05),但没有明显新生肿瘤血管;荷瘤2w及3w组肿瘤区CBF,BV,PS值和瘤脑交界处PS值均比对侧正常脑组织明显增大,肿瘤中心、肿瘤周边和瘤脑交界处之间仅PS值差别具有统计学意义,肿瘤区微血管密度(MVD)值明显增大,以肿瘤周边更为明显,其差别具有统计学意义(P<0.05);整个观察期内肿瘤中心和周边区域CBV值及肿瘤中心PS值与相应的MVD值呈等级正相关,rs分别为0.576、0.482和0.646(P<0.05)。结论:CT灌注成像可以反映大鼠C6脑胶质瘤生长过程中肿瘤区域不同部位微循环的动态变化,其中肿瘤周边区域CBV和PS值变化明显,反映了血管生成。