scholarly journals Effect of combined treatment with X-irradiation and 5-fluorouracil in multicellular spheroids of rat glioma.

1987 ◽  
Vol 27 (12) ◽  
pp. 1139-1146 ◽  
Author(s):  
Kenji KUWAHARA ◽  
Ryuichi KATAKURA ◽  
Teruaki MORI ◽  
Jiro SUZUKI ◽  
Takehito SASAKI
Keyword(s):  
Combined Treatment ◽  
Multicellular Spheroids ◽  
Rat Glioma ◽  
X Irradiation

Effect of Combined Treatment of X-rays and A CNU on Rat Glioma Cells in Monolayer and Multicellular Spheroids

1985 ◽  
Vol 25 (9) ◽  
pp. 707-714 ◽  
Author(s):  
Satoru SUGIYAMA ◽  
Teruaki MORI ◽  
Jiro SUZUKI ◽  
Takehito SASAKI
Keyword(s):  
Combined Treatment ◽  
Glioma Cells ◽  
X Rays ◽  
Multicellular Spheroids ◽  
Rat Glioma

scholarly journals Effect of Chemical Protection and Bone Marrow Treatment on Radiation Injury in Mice

Blood ◽  
1958 ◽  
Vol 13 (7) ◽  
pp. 665-676 ◽  
Author(s):  
PAUL URSO ◽  
C. C. CONGDON ◽  
D. G. DOHERTY ◽  
RAYMOND SHAPIRA
Keyword(s):  
Bone Marrow ◽  
Body Weight ◽  
Radiation Injury ◽  
Combined Treatment ◽  
X Rays ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Hematopoietic Organs ◽  
X Irradiation ◽  
Bone Marrow Granulocytes

Abstract MEG (prepared from 9.0 mg. of AET) significantly modified the response of the bone marrow, peripheral blood leukocytes, spleen, thymus, body weight, hematocrit, and histology of the hematopoietic organs to lethal (900 r) and sublethal (450 r) x-irradiation in CAF1 mice. MEG reduced the effect of 900 r on the bone marrow, granulocytes of the blood, hematocrit, spleen, thymus, and body weight by a factor of approximately two. Combined treatment (MEG and isologous bone marrow) of mice exposed to 900 r of x-rays demonstrated that MEG is primarily responsible for preventing the early destruction of the bone marrow, but bone marrow injection was primarily responsible for causing a more rapid recovery of the bone marrow. In mice receiving combined treatment, recovery of the leukocytes and spleen was primarily influenced by the bone marrow injection; whereas recovery of the thymus and body weight was primarily influenced by MEG. The hematocrit values were normal after combined treatment.

scholarly journals Lethal Effect of X-ray and ACNU on Cultured Rat Glioma Cells in Multicellular Spheroids

1984 ◽  
Vol 24 (10) ◽  
pp. 758-766 ◽  
Author(s):  
Satoru SUGIYAMA ◽  
Teruaki MORI ◽  
Jiro SUZUKI ◽  
Takehito SASAKI
Keyword(s):  
Glioma Cells ◽  
Lethal Effect ◽  
Multicellular Spheroids ◽  
X Ray ◽  
Rat Glioma

scholarly journals Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Sonja Stojković Burić ◽  
Ana Podolski-Renić ◽  
Jelena Dinić ◽  
Tijana Stanković ◽  
Mirna Jovanović ◽  
...  
Keyword(s):  
Coenzyme Q10 ◽  
Glioma Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Combined Treatment ◽  
Glioma Cell Line ◽  
Mesenchymal Transition ◽  
Rat Glioma ◽  
Matrigel Invasion

The main reasons for the inefficiency of standard glioblastoma (GBM) therapy are the occurrence of chemoresistance and the invasion of GBM cells into surrounding brain tissues. New therapeutic approaches obstructing these processes may provide substantial survival improvements. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) as a scavenger of reactive oxygen species (ROS) to increase sensitivity to temozolomide (TMZ) and suppress glioma cell invasion. To that end, we used a previously established TMZ-resistant RC6 rat glioma cell line, characterized by increased production of ROS, altered antioxidative capacity, and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic antiproliferative effect. These results were confirmed in a 3D model of microfluidic devices showing that the CoQ10 and TMZ combination is more cytotoxic to RC6 cells than TMZ monotherapy. In addition, cotreatment with TMZ increased expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential of the combined treatment was shown by gelatin degradation, Matrigel invasion, and 3D spheroid invasion assays as well as in animal models. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, our data provide evidences in favor of CoQ10 supplementation to standard GBM treatment due to its potential to inhibit GBM invasion through modulation of the antioxidant capacity.

scholarly journals Somatostatin Receptors 1, 2, and 5 Cooperate in the Somatostatin Inhibition of C6 Glioma Cell Proliferation in Vitro via a Phosphotyrosine Phosphatase-η-Dependent Inhibition of Extracellularly Regulated Kinase-1/2

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4736-4746 ◽  
Author(s):  
Federica Barbieri ◽  
Alessandra Pattarozzi ◽  
Monica Gatti ◽  
Carola Porcile ◽  
Adriana Bajetto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Antiproliferative Activity ◽  
Combined Treatment ◽  
Somatostatin Receptors ◽  
Receptor Activation ◽  
Phosphotyrosine Phosphatase ◽  
Rat Glioma ◽  
Simultaneous Activation ◽  
The Individual

Somatostatin inhibits cell proliferation through the activation of five receptors (SSTR1–5) expressed in normal and cancer cells. We analyzed the role of individual SSTRs in the antiproliferative activity of somatostatin in C6 rat glioma cells. Somatostatin dose-dependently inhibited C6 proliferation, an effect mimicked, with different efficacy or potency, by BIM-23745, BIM-23120, BIM-23206 (agonists for SSTR1, -2, and -5) and octreotide. The activation of SSTR3 was ineffective, although all SSTRs are functionally active, as demonstrated by the inhibition of cAMP production. All SSTRs induced cytostatic effects through the activation of the phosphotyrosine phosphatase PTPη and the inhibition of ERK1/2. For possible synergism between SSTR subtypes, we tested the effects of the combined treatment with two agonists (SSTR1+2 or SSTR2+5) or bifunctional compounds. The simultaneous activation of SSTR1 and SSTR2 slightly increased the efficacy of the individual compounds with an IC50 in between the single receptor activation. SSTR2+5 activation displayed a pattern of response superimposable to that of the SSTR5 agonist alone (low potency and higher efficacy, as compared with BIM-23120). The simultaneous activation of SSTR1, -2, and -5 resulted in a response similar to somatostatin. In conclusion, the cytostatic effects of somatostatin in C6 cells are mediated by the SSTR1, -2, and -5 through the same intracellular pathway: activation of PTPη and inhibition of ERK1/2 activity. Somatostatin is more effective than the individual agonists. The combined activation of SSTR1 and -2 shows a partial synergism as far as antiproliferative activity, whereas SSTR2 and -5 activation results in a response resembling the SSTR5 effects.

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