scholarly journals Effect of Different Isorhamnetin of Different Density Cultured Rat C6 Glioma Cells in Vitro

2018 ◽  
Vol 2 (1) ◽  
Author(s):  
Jinhua Yang ◽  
Zhuanni Sun
Keyword(s):  
Survival Rate ◽  
Brain Tissue ◽  
High Performance ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Control Group ◽  
Brain Glioma ◽  
Apoptosis And Necrosis

Objective To explore the influence of different concentrations of isorhamnetin on C6 glioma cell morphology. Methods Set the blank control group, blank solvent control group and reagent group of four concentration, the growth of cells were observed under microscope; MTT assay was used to test the effect of isorhamnetin on cultured C6 glioma cells, as well as calculate the cell inhibition rate and survival rate; flow cytometry was used to check the detection peak and detection rate of Isorhamnetin group and negative control apoptosis group, and analyzed the relationship between different concentrations of isorhamnetin and C6 glioma cell apoptosis rate; total protein was extracted from cells, and used Western blotting to detected total AKT protein and Ser473 AKT protein loci in cells; used SD rats to construct brain glioma model, feed isorhamnetin plain to them for five days, and then used HPLC to detect plasma, liver, brain tissue content. Results Under the observation of inverted microscope and image analysis, after using Isorhamnetin, tumor cells appear apoptosis and necrosis change. Display with different Isorhamnetin MTT colorimetric method shows that the higher the concentration of added Isorhamnetin, the worse the growth rate of C6 glioma cells in vitro, and the higher the Inhibitory rate, the lower survival rate. The flow cytometric detection shows the C6 glioma cells which is added 40 ug/ul Isorhamnetin have the highest rate of apoptosis. After adding 80 μ g/ μ l concentration of the isorhamnetin, C6 glioma cells have the lowest survival rate. Western blot test shows the AKT protein and Ser473 total site AKT protein density is in reverse proportion to the increase of the concentration of the isorhamnetin. High performance liquid chromatographic method has determined that there are isorhamnetin in both the rat plasma and brain tissue, which shows that the plasma and tissue all have different isorhamnetin  distribution,  and  isorhamnetin mainly exist in the brain tissue. Conclusion Low concentration  of  isorhamnetin  can  induce apoptosis  of  C6  glioma  cells,  and  high concentration of isorhamnetin can lead to apoptosis and necrosis of C6 glioma cells in vitro, which has obvious inhibitory effect on the growth of glioma cells, and the mechanism is closely related to PI3K/AKT pathway, and in SD rat brain glioma model , the high performance liquid chromatography was used to detect the content of plasma and brain tissue, which indicated the isorhamnetin has target in brain tissue, which provided  experimental  evidence  for  the development and utilization of isorhamnetin in mice.

scholarly journals Effect of Rat C6 Glioma Cells in Varying Concentrations of Cultured in Isorhamnetin

1970 ◽  
Vol 1 (1) ◽  
Author(s):  
TIAN Rui-rui
Keyword(s):  
High Performance ◽  
Colorimetric Assay ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Control Group ◽  
Blank Control Group ◽  
Rat Glioma ◽  
Solvent Control

Objective: To investigate the effects of different concentrations of isorhamnetin on C6 rat glioma cells in vitro from January 2015 to June 2015. Methods: The blank control group, blank solvent control group and four concentration groups were used to observe the cell growth status under a microscope. MTT colorimetric assay was used to detect the effect of isorhamnetin on C6 glioma cells in vitro and the cell inhibition rate And survival rate were measured. The apoptotic and apoptotic rates were measured by flow cytometry in the treatment group and the control group. The relationship between the different concentrations of isorhamnetin and C6 glioma cell apoptosis was analyzed the total protein was extracted and the total AKT protein and Ser473 AKT protein content were detected by Western blotting. The rat model of glioma was constructed by SD rats.Five days of isorhamnetin was continuously fed and the plasma was detected by high-performance liquid chromatography,liver, brain tissue isorhamnetin content. 

Radiosensitivity of glioma to Gamma Knife treatment enhanced in vitro and in vivo by RNA interfering Ku70 that is mediated by a recombinant adenovirus

2010 ◽  
Vol 113 (Special_Supplement) ◽  
pp. 228-235 ◽  
Author(s):  
Qiang Jia ◽  
Yanhe Li ◽  
Desheng Xu ◽  
Zhenjiang Li ◽  
Zhiyuan Zhang ◽  
...  
Keyword(s):  
Western Blot ◽  
Gamma Knife ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells

Object The authors sought to evaluate modification of the radiation response of C6 glioma cells in vitro and in vivo by inhibiting the expression of Ku70. To do so they investigated the effect of gene transfer involving a recombinant replication-defective adenovirus containing Ku70 short hairpin RNA (Ad-Ku70shRNA) combined with Gamma Knife treatment (GKT). Methods First, Ad-Ku70shRNA was transfected into C6 glioma cells and the expression of Ku70 was measured using Western blot analysis. In vitro, phenotypical changes in C6 cells, including proliferation, cell cycle modification, invasion ability, and apoptosis were evaluated using the MTT (3′(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide) assay, Western blot analysis, and cell flow cytometry. In vivo, parental C6 cells transfected with Ad-Ku70shRNA were implanted stereotactically into the right caudate nucleus in Sprague-Dawley rats. After GKS, apoptosis was analyzed using the TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling) method. The inhibitory effects on growth and invasion that were induced by expression of proliferating cell nuclear antigen and matrix metalloproteinase–9 were determined using immunohistochemical analyses. Results The expression of Ku70 was clearly inhibited in C6 cells after transfection with Ad-Ku70shRNA. In vitro following transfection, the C6 cells showed improved responses to GKT, including suppression of proliferation and invasion as well as an increased apoptosis index. In vivo following transfection of Ad-Ku70shRNA, the therapeutic efficacy of GKT in rats with C6 gliomas was greatly enhanced and survival times in these animals were prolonged. Conclusions Our data support the potential for downregulation of Ku70 expression in enhancing the radiosensitivity of gliomas. The findings of our study indicate that targeted gene therapy–mediated inactivation of Ku70 may represent a promising strategy in improving the radioresponsiveness of gliomas to GKT.

Significant correlations between atmospheric spectra according to Baumer and the in vitro incorporation of [3 H]thymidine into the nuclear DNA of C6-glioma cells

FEBS Letters ◽  
1991 ◽  
Vol 288 (1-2) ◽  
pp. 244-246 ◽  
Author(s):  
Siegfried Vogl ◽  
Georg Hoffmann ◽  
Barbara Stöpfel ◽  
Hans Baumer ◽  
Oliver Kempski ◽  
...  
Keyword(s):  
Nuclear Dna ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells

Synergistic Apoptotic Effect of Naringenin on enhancing the Anti-Glioma Efficacy of Temozolomide in an in vitro Experimental Model

2021 ◽  
Vol 16 (10) ◽  
pp. 43-49
Author(s):  
Precilla S. Daisy ◽  
S. Kuduvalli Shreyas ◽  
R. Sathish ◽  
T.S. Anitha
Keyword(s):  
Drug Treatment ◽  
Caspase 3 ◽  
Treatment Strategies ◽  
Glioma Cells ◽  
C6 Glioma ◽  
Mitigation Strategies ◽  
Treatment Modalities ◽  
C6 Glioma Cells ◽  
Dependent Manner

Glioma is one of the most devastating and difficult-totreat brain tumors with a very poor prognosis. Despite the current treatment modalities, the overall survival rate is only 5% contributing to a high mortality rate. Nevertheless, of emerging treatment strategies, there is still a rising need for novel mitigation strategies to counteract glioma aggressiveness. One attempt towards this long-term goal was made in this study to reveal the combined efficacy of naringenin, a bioactive flavonoid on enhancing the anti-glioma potency of temozolomide in C6 glioma cells. The cytotoxic effect of temozolomide and naringenin, both individually and in combination was assessed by employing MTT assay. The synergistic effect of the drugs temozolomide and naringenin was determined by calculating the combination index. To confirm the presence of apoptotic changes in the cells at morphological level, acridine orange/ethidium bromide staining was performed. Further, the modulatory effects of the drugs on apoptotic genes, caspase-3 and BCL-2 were evaluated using quantitative real time-PCR. Interestingly, we found that the combinatorial drug treatment was in consensus and effectively inhibited the growth of C6 glioma cells in a dose-dependent manner. Furthermore, this combinatorial drug treatment significantly up-regulated the expression of the proapoptotic gene, caspase-3 and down-regulated the anti-apoptotic gene BCL-2 suggesting a shift of equilibrium towards apoptosis. Our findings suggest that naringenin can be employed as a potent drug to enhance the anti-glioma efficacy of temozolomide and could be therapeutically exploited for the management of glioma.

scholarly journals Membrane-type 1 Matrix Metalloprotease (MT1-MMP) Enables Invasive Migration of Glioma Cells in Central Nervous System White Matter

1999 ◽  
Vol 144 (2) ◽  
pp. 373-384 ◽  
Author(s):  
Ann T.J. Beliën ◽  
Paolo A. Paganetti ◽  
Martin E. Schwab
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
White Matter ◽  
Plasma Membranes ◽  
Malignant Gliomas ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Glioblastoma Cells

Invasive glioma cells migrate preferentially along central nervous system (CNS) white matter fiber tracts irrespective of the fact that CNS myelin contains proteins that inhibit cell migration and neurite outgrowth. Previous work has demonstrated that to migrate on a myelin substrate and to overcome its inhibitory effect, rat C6 and human glioblastoma cells require a membrane-bound metalloproteolytic activity (C6-MP) which shares several biochemical and pharmacological characteristics with MT1-MMP. We show now that MT1-MMP is expressed on the surface of rat C6 glioblastoma cells and is coenriched with C6-MP activity. Immunodepletion of C6-MP activity is achieved with an anti–MT1-MMP antibody. These data suggest that MT1-MMP and the C6-MP are closely related or identical. When mouse 3T3 fibroblasts were transfected with MT1-MMP they acquired the ability to spread and migrate on the nonpermissive myelin substrate and to infiltrate into adult rat optic nerve explants. MT1-MMP–transfected fibroblasts and C6 glioma cells were able to digest bNI-220, one of the most potent CNS myelin inhibitory proteins. Plasma membranes of both MT1-MMP–transfected fibroblasts and C6 glioma cells inactivated inhibitory myelin extracts, and this activity was sensitive to the same protease inhibitors. Interestingly, pretreatment of CNS myelin with gelatinase A/MMP-2 could not inactivate its inhibitory property. These data imply an important role of MT1-MMP in spreading and migration of glioma cells on white matter constituents in vitro and point to a function of MT1-MMP in the invasive behavior of malignant gliomas in the CNS in vivo.

Wild Type p53 Gene Sensitizes Rat C6 Glioma Cells to HSV-TK/ACV Treatment In Vitro and In Vivo

2010 ◽  
Vol 16 (4) ◽  
pp. 509-514 ◽  
Author(s):  
Qiang Huang ◽  
Zhibo Xia ◽  
Yongping You ◽  
Peiyu Pu
Keyword(s):  
Glioma Cells ◽  
P53 Gene ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Wild Type ◽  
Wild Type P53 ◽  
Rat C6 Glioma

In vitro study of haematoporphyrin monomethyl ether-mediated sonodynamic effects on C6 glioma cells

2008 ◽  
Vol 29 (4) ◽  
pp. 229-235 ◽  
Author(s):  
Jian-hua Li ◽  
Da-yong Song ◽  
Yong-gang Xu ◽  
Zheng Huang ◽  
Wu Yue
Keyword(s):  
Glioma Cells ◽  
In Vitro Study ◽  
Monomethyl Ether ◽  
C6 Glioma ◽  
Vitro Study ◽  
C6 Glioma Cells
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