dinoprost and thiazolyl-blue

To evaluate the effect of TEGDMA on cell cycle progression as well as alterations of cell cycle-related gene and protein expression.. Human dental pulp cells were exposed to 0-5 mmol L(-1) TEGDMA for 24 h. Cytotoxicity was evaluated by 3-(4, 5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Cell cycle progression was analysed by propidium iodide (PI) flow cytometry. Cell death pathway was surveyed by annexin V/PI dual-staining flow cytometry. The mRNA expression of cell cycle-related genes (cdc2, cyclinB1 and p21) and COX-2 was evaluated by reverse transcriptase-polymerase chain reaction, and their protein expression was evaluated by Western blotting. The production of PGE(2) and PGF(2α) in the culture medium was determined by enzyme-linked immunosorbent assay.. Triethylene glycol dimethacrylate inhibited cellular growth and induced cell cycle deregulation in dental pulp cells. High-dose exposure provoked both necrotic and apoptotic cell death. The gene and protein expression of cdc2, cyclin B1 and cdc25C declined obviously whilst cells treated with 2.5 mmol L(-1) TEGDMA concurrent with the elevated expression of p21. The mRNA and protein expression of COX-2, along with production of PGE(2) and PGF(2α), are drastically raised by 2.5-5 mmol L(-1) TEGDMA.. Triethylene glycol dimethacrylate induced cytotoxicity, cell cycle arrest and apoptosis in dental pulp cells, which was associated with the decline of cdc2, cyclin B1, cdc25C expression and elevation of p21 expression. Concomitantly, COX-2 expression, PGE(2) and PGF(2α) production increased. These effects may contribute to explain the pulpal damage and inflammation induced by TEGDMA after operative procedures.

Topics: Annexin A5; Apoptosis; CDC2 Protein Kinase; cdc25 Phosphatases; Cell Culture Techniques; Cell Cycle; Cell Death; Cell Proliferation; Cell Shape; Coloring Agents; Cyclin B; Cyclin B1; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinases; Cyclooxygenase 2; Dental Materials; Dental Pulp; Dinoprost; Dinoprostone; Enzyme Inhibitors; Flow Cytometry; Fluorescein-5-isothiocyanate; Fluorescent Dyes; Humans; Necrosis; Polyethylene Glycols; Polymethacrylic Acids; Propidium; Prostaglandins; Tetrazolium Salts; Thiazoles; Time Factors

Nitroxyl (HNO) donor compounds function as potent vasorelaxants, improve myocardial contractility and reduce ischemia-reperfusion injury in the cardiovascular system. With respect to the nervous system, HNO donors have been shown to attenuate NMDA receptor activity and neuronal injury, suggesting that its production may be protective against cerebral ischemic damage. Hence, we studied the effect of the classical HNO-donor, Angeli's salt (AS), on a cerebral ischemia/reperfusion injury in a mouse model of experimental stroke and on related in vitro paradigms of neurotoxicity. I.p. injection of AS (40 mumol/kg) in mice prior to middle cerebral artery occlusion exacerbated cortical infarct size and worsened the persistent neurological deficit. AS not only decreased systolic blood pressure, but also induced systemic oxidative stress in vivo indicated by increased isoprostane levels in urine and serum. In vitro, neuronal damage induced by oxygen-glucose-deprivation of mature neuronal cultures was exacerbated by AS, although there was no direct effect on glutamate excitotoxicity. Finally, AS exacerbated oxidative glutamate toxicity - that is, cell death propagated via oxidative stress in immature neurons devoid of ionotropic glutamate receptors. Taken together, our data indicate that HNO might worsen cerebral ischemia-reperfusion injury by increasing oxidative stress and decreasing brain perfusion at concentrations shown to be cardioprotective in vivo.

Topics: Animals; Blood Pressure; Brain Infarction; Cells, Cultured; Dinoprost; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interactions; Enzyme-Linked Immunosorbent Assay; F2-Isoprostanes; Gas Chromatography-Mass Spectrometry; Glutamic Acid; Infarction, Middle Cerebral Artery; L-Lactate Dehydrogenase; Mice; Mice, Inbred C57BL; Neuroglia; Neurons; Neuroprotective Agents; Nitrites; Nitrogen Oxides; Oxidative Stress; Statistics, Nonparametric; Tetrazolium Salts; Thiazoles; Time Factors