九节龙皂苷Ⅰ对胶质瘤U87细胞侵袭和迁移的影响

目的 观察九节龙皂苷Ⅰ(从九节龙全草中萃取)对胶质瘤U87细胞体外侵袭、迁移等生物学行为的影响及作用机制的探讨.方法 体外培养U87细胞,采用四甲基偶氮唑蓝(MTT)实验检测胶质瘤U87细胞经不同浓度九节龙皂苷Ⅰ作用24、48、72 h后增殖率的变化;细胞划痕实验观察九节龙皂苷Ⅰ对U87细胞移动能力的影响;Transwell侵袭转移模型评价九节龙皂苷Ⅰ对U87细胞侵袭能力的影响;明胶酶谱法分析九节龙皂苷Ⅰ对U87细胞分泌基质金属蛋白酶(MMP)活性的影响.结果 MTT法显示一定浓度的九节龙皂苷Ⅰ可抑制U87细胞生长,并随着浓度增加和作用时间延长而明显增加(P＜0.05);与对照组比较,经九节龙皂苷Ⅰ作用后U87细胞迁移和侵袭能力明显降低,MMP-2分泌减少.结论 九节龙皂苷Ⅰ可有效抑制脑胶质瘤U87细胞迁移和侵袭能力,其机制可能与九节龙皂苷Ⅰ降低细胞MMP-2活性相关.     

Increasing nodal vulnerability and nodal efficiency implied recovery time prolonging in patients with supplementary motor area syndrome

Supplementary motor area (SMA) syndrome is a surgery‐related complication that commonly occurs after removing SMA glioma, and needs weeks to recover. However, susceptible factors of patients suffering from SMA syndrome remain unknown. Graphic theory was applied to reveal topological properties of sensorimotor network (SMN) by processing resting‐state functional magnetic resonance images in 66 patients with SMA gliomas. Patients were classified into SMA and non‐SMA groups based on whether they suffered from SMA syndrome. We collected recovery time and used causal mediation analysis to find association between topological properties and recovery time. Compared with the non‐SMA group, higher vulnerability (left: p = .0018; right: p = .0033) and lower fault tolerance (left: p = .0022; right: p = .0248) of the whole SMN were found in the SMA group. Moreover, higher nodal properties of lesional‐hemispheric cingulate cortex (nodal efficiency: left, p = .0389; right, p = .0169; nodal vulnerability: left, p = .0185; right, p = .0085) and upper limb region of primary motor cortex (PMC; nodal efficiency: left, p = .0132; right, p = .0001; nodal vulnerability: left, p = .0091; right, p = .0209) were found in the SMA group. Nodal efficiency and nodal vulnerability of cingulate cortex and upper limb region of PMC were important predictors for SMA syndrome occurring and recovery time prolonging. Neurosurgeons should carefully deal with upper limb region of PMC and cingulate cortex, and protect them if these two region were unnecessary to damage during SMA glioma resection.     

胶质瘤3D ASL 灌注指数与VEGF MVD 表达相关性研究

目的:探究胶质瘤磁共振三维动脉自旋标记成像（three dimensional arterial spin labeling,3DASL）肿瘤实质相对血流量（relative cerebral blood flow ,rCBF）与血管内皮生长因子（vascular endothelia lgrowth factor,VEGF）、微血管密度（micro vessel density,MVD）表达程度的相关性。方法:回顾性分析沈阳军区总医院2014年8 月至2016年2 月53例经术后病理证实的胶质瘤患者,术前行MR平扫、增强、3DASL扫描,术后行VEGF、MVD表达程度检测,分析胶质瘤肿瘤实质rCBF与VEGF、MVD表达的关系。结果:胶质瘤肿瘤实质rCBF分别与VEGF、MVD表达呈正相关（r s 值分别为0.728、0.620,P < 0.05）。 结论:胶质瘤肿瘤实质rCBF值与VEGF、MVD表达呈正相关,说明3DASL灌注成像技术有助于评估胶质瘤微血管生成情况,对临床制定适当的治疗计划和患者预后评估有一定意义。      

Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit in vitro

Aim:

To examine the effects of anisomycin on glioma cells and the related mechanisms in vitro.

Methods:

The U251 and U87 human glioblastoma cell lines were tested. The growth of the cells was analyzed using a CCK-8 cell viability assay. Apoptosis was detected using a flow cytometry assay. The expression of proteins and phosphorylated kinases was detected using Western blotting.

Results:

Treatment of U251 and U87 cells with anisomycin (0.01–8 μmol/L) inhibited the cell growth in time- and concentration-dependent manners (the IC₅₀ values at 48 h were 0.233±0.021 and 0.192±0.018 μmol/L, respectively). Anisomycin (4 μmol/L) caused 21.5%±2.2% and 25.3%±3.1% of apoptosis proportion, respectively, in U251 and U87 cells. In the two cell lines, anisomycin (4 μmol/L) activated p38 MAPK and JNK, and inactivated ERK1/2. However, neither the p38 MAPK inhibitor SB203580 (10 μmol/L) nor the JNK inhibitor SP600125 (10 μmol/L) prevented anisomycin-induced cell death. On the other hand, anisomycin (4 μmol/L) reduced the level of PP2A/C subunit (catalytic subunit) in a time-dependent manner in the two cell lines. Treatment of the two cell lines with the PP2A inhibitor okadaic acid (100 nmol/L) caused marked cell death.

Conclusion:

Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit. The regulation of PP2A/C exression by anisomycin provides a clue to further study on its role in glioma therapy.     

脑胶质瘤中单酰甘油脂肪酶的表达及意义

目的 研究内源性大麻素代谢酶单酰甘油脂肪酶（monoacylglycerol lipase,MAGL）在脑胶质瘤组织中的表达情况及其与胶质瘤病理级别的关系,探讨其临床意义。方法 选取脑胶质瘤标本23例,其中WHO Ⅰ级1例,WHO Ⅱ级7例,WHO Ⅲ级5例,WHO Ⅳ级10例。对照组8例,均为脑挫裂伤后行内减压术切除的正常脑组织。应用实时荧光定量PCR（qRT-PCR）、LC-MS分别检测各组织标本中MAGL mRNA、MAGL活性的表达。结果 MAGL mRNA、MAGL活性在低级别（WHOⅠ~Ⅱ级）和高级别（WHOⅢ~Ⅳ级）脑胶质瘤组织中的表达水平较正常脑组织明显降低（P<0.01）,且随着肿瘤病理级别的增高而降低,与肿瘤的病理分级呈负相关（均P<0.01）。MAGL mRNA的表达水平与MAGL活性呈正相关。结论 MAGL可能参与了脑胶质瘤的发生、发展过程,检测MAGL的表达可评价脑胶质瘤的恶性程度。     

羟基脲对人脑胶质瘤U251细胞放化疗增敏作用的研究

目的:探讨羟基脲(HU)联合替莫唑胺(TMZ)加放疗(RT)对人脑胶质瘤U251细胞放化疗(CRT)敏感性的影响。方法:体外培养U251细胞,采用CCK8实验检测不同浓度HU、TMZ及不同条件处理后细胞的增殖能力;流式细胞术检测细胞凋亡及细胞周期分布情况;Transwell小室、划痕实验评估细胞侵袭、迁移能力变化;We...     

术中MR液体反转恢复序列在低级别神经胶质瘤切除术中的应用价值

目的 探讨术中磁共振成像(intraoperative MRI,iMRI)中的液体反转恢复序列(fluid attenuated inversion recovery,FLAIR)在低级别神经胶质瘤(WHO Ⅰ～Ⅱ级)切除术中的应用价值,从而对是否存在残留肿瘤的诊断提供帮助.方法 选取18例低级别神经胶质瘤(low-g...     

XBP1 对低氧环境下胶质瘤细胞活力及糖酵解的影响*

目的：明确低氧应激对胶质瘤细胞X-盒结合蛋白1（X-box binding protein1,XBP 1）的作用;明确胶质瘤细胞XBP 1 表达与糖代谢之间的关系;抑制XBP 1 表达对胶质瘤细胞在常氧和低氧环境下细胞活力的影响;明确低氧环境中XBP 1 对胶质瘤细胞糖酵解的影响。方法：分别在常氧和低氧条件下培养人脑胶质瘤细胞系,检测XBP 1 激活情况;使用siRNA 技术抑制XBP 1 表达,使用氧化磷酸化抑制剂处理细胞,检测细胞活力及糖代谢方式的改变,在常氧和低氧条件下检测细胞存活及糖酵解产物。结果：低氧环境下XBP 1 活化增加。低氧环境下XBP 1 沉默降低胶质瘤细胞活力、ATP 和乳酸生成,葡萄糖消耗量减少。细胞氧化磷酸化受到抑制后,XBP 1 沉默降低胶质瘤细胞存活率。结论：低氧环境可诱导胶质瘤细胞XBP 1 的活化。在低氧环境下XBP 1 沉默降低胶质瘤细胞活力和糖酵解,胶质瘤细胞的糖酵解依赖于XBP 1 活化。