ABSTRACT
Objective To investigate the apoptosis of rat glioma C 6 cells induced by defective in-terfering( DI) particles of Sendai virus strain Tianjin .Methods Rat glioma C6 cells were treated with dif-ferent titers of DI particles of Sendai virus strain Tianjin in vitro with culture media as negative control and intact virus as positive control .At different time point , cells were collected and their apoptosis was detected by DNA gel electrophorsis , TUNEL assay and AnnexinⅤ/PI double-labeled flow cytometry .The C6 glioma-bearing rat model was established and then treated with three intratumoral injections of DI particles , intact virus or saline three times at interval of two days .The antitumor effects of ID particles were evaluated through daily measuring of the tumor size .Hematoxylin-eosin( HE) staining was used to observe the patho-logical changes in tumor tissues .TUNEL assay was performed to detect the apoptosis of tumor tissues .Re-sults Rat glioma C6 cells treated with DI particles or intact virus in vitro showed typical DNA ladder pattern in agarose gel electrophoresis in a time-and dose-dependent manner .With the intervention of DI particles , the apoptosis rate of C6 cells showed a time-and dose-dependent manner and was significantly higher than that of the control group (P0.05).Conclusion The DI particles of Sendai virus strain Tianjin could induce apoptosis of rat glioma C 6 cells in a time-and dose-dependent manner both in vitro and in vivo, suggesting that the DI particles might be applicable for the treatment of neurogliocytoma in the future.
ABSTRACT
Objetives: Identification of target genes for ethanol in neurons is important for understanding its molecular and cellular mechanism of action and the neuropathological changes seen in alcoholics. The purpose of this study is to identify of altered gene expression after acute treatmet of ethanol in rat gliom cells. METHODS: We used high density cDNA microarray chip to measure the expression patterns of multiple genes in cultured rat glioma cells. DNA microarrays allow for the simultaneous measurement of the expression of several hundreds of genes. RESULTS: After comparing hybridized signals between control and ethanol treated groups, we found that treatment with ethanol increased the expression of 15 genes and decreased the expression of 12 genes. Upregulated genes included Orthodenticle(Drosophila) homolog 1, procollagen type II, adenosine A2a receptor, GATA-bindning protein 2. Downregulated genes included diacylglycerol kinase beta, PRKC, Protein phosphatase 1, clathrin-associated protein 17, nucleoporin p58, proteasome. CONCLUSION: The gene changes noted were those related to the regulation of transcription, signal transduction, second messenger systems. modulation of ischemic brain injury, and neurodengeneration.Although some of the genes were previously known to be ethanol responsive, we have for the most part identified novel genes involved in the brain response to ethanol.
Subject(s)
Animals , Humans , Rats , Alcoholics , Brain , Brain Injuries , Collagen Type II , Diacylglycerol Kinase , Ethanol , Gene Expression , Glioma , Microarray Analysis , Neurons , Nuclear Pore Complex Proteins , Oligonucleotide Array Sequence Analysis , Proteasome Endopeptidase Complex , Protein Phosphatase 1 , Receptor, Adenosine A2A , Second Messenger Systems , Signal TransductionABSTRACT
Aim To study the effect of saikogenin d (SGD) on prostaglandin E 2(PGE 2) production in C 6 rat glioma cells. Methods Radioimmunoassay was applied to determine PGE 2 production in the cells. Scintillation counting was used to measure liberation of -arachidonic acid (AA) from the cells labeled with -AA. Results In vitro, SGD alone at 1～20 ?mol?L -1 did not affect PGE 2 release from cells, but inhibited its release induced by A23187, a Ca 2+ ionophore. The inhibition was concentration-dependent, with the IC 50 value of about 3 ?mol?L -1. SGD (2～10 ?mol?L -1 ) had no inhibitory effect on A23187-induced AA release or on the conversion of AA to PGE 2 in microsomal preparations. Conclusion SGD inhibites A23187-induced PGE 2 production in C 6 rat glioma cells in vitro, without either inhibition of free AA liberation or a direct inhibition of cyclooxygenase (COX) activity.