ABSTRACT
BACKGROUND: Dual source computed tomography (DSCT) plays an important role in the diagnosis of congenital heart diseases (CHD). However, the issue of radiation-related side effects constitutes a wide public concern. The aim of the study was to explore the differences in diagnostic accuracy, radiation dose and image quality between a prospectively ECG - triggered high - pitch spiral acquisition (flash model) and a retrospective ECG-gated protocol of DSCT used for the detection of CHD. MATERIAL/METHODS: The study included 58 patients with CHD who underwent a DSCT examination, including two groups of 29 patients in each protocol. Then, both subjective and objective image quality, diagnostic accuracy and radiation dose were compared between the two protocols. RESULTS: The image quality and the total as well as partial diagnostic accuracy did not differ significantly between the protocols. The radiation dose in the flash model was obviously lower than that in the retrospective model (P<0.05). CONCLUSIONS: Compared to the retrospective protocol, the flash model can significantly reduce the dose of radiation, while maintaining both diagnostic accuracy and image quality.
ABSTRACT
The aim of this study was to investigate the protective effects of Mimic of Manganese superoxide dismutase (MnSODm) against carbon tetrachloride (CCl(4))-induced hepatic injury in mice. Bifendate or MnSODm was intragastrically administered per day for 7 days. On the 8th day, all mice except the normal group were given 0.5% CCl(4)/peanut oil to induce hepatic injury model by intraperitoneal injection. Mice were sacrificed 24 h after CCl(4) treatment. Compared with the CCl(4) group, MnSODm significantly decreased the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the serum and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the serum and liver. Moreover, the contents of hepatic and serum malondialdehyde (MDA) and nitric oxide (NO) with inducible nitric oxide synthase (iNOS) activities were reduced. Histological findings also confirmed the antihepatotoxic characterization. In addition, MnSODm inhibited the pro-inflammatory mediators, such as prostaglandin E(2) (PGE(2)), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Further investigation showed that the inhibitory effect of MnSODm on the pro-inflammatory cytokines was associated with the down-regulation of nuclear factor-kappa B (NF-κB). In brief, our results show that the protective effect of MnSODm against CCl(4)-induced hepatic injury may rely on its ability to reduce oxidative stress and suppress inflammatory responses.
Subject(s)
Biomimetic Materials/administration & dosage , Biphenyl Compounds/administration & dosage , Chemical and Drug Induced Liver Injury/immunology , Liver/drug effects , Superoxide Dismutase/metabolism , Alanine Transaminase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Biomimetic Materials/chemistry , Carbon Tetrachloride/administration & dosage , Chemical and Drug Induced Liver Injury/drug therapy , Cyclooxygenase 2/metabolism , Glutathione Peroxidase/metabolism , Heterocyclic Compounds, 4 or More Rings/administration & dosage , Heterocyclic Compounds, 4 or More Rings/chemistry , Inflammation Mediators/metabolism , Interleukin-6/metabolism , Liver/metabolism , Liver/pathology , Male , Malondialdehyde/metabolism , Mice , Mice, Inbred Strains , NF-kappa B/genetics , NF-kappa B/metabolism , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/metabolism , Oxidative Stress/drug effects , Superoxide Dismutase/chemistry , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Abstract Increasing manganese superoxide dismutase (MnSOD) expression can suppress the malignant phenotype in various cancer cell lines and suppress tumor formation in xenograft and transgenic mouse models. A mimic of manganese superoxide dismutase (MnSODm), synthesized by a chemical method, has been shown to possess antitumor properties. However, the anticancer activity of MnSODm in acute myeloid leukemia (AML) is still obscure. In this study, we investigated the effects of MnSODm on the apoptosis of human leukemia HL-60 cells. Results showed that MnSODm significantly reduced the proliferation of HL-60 cells in a concentration- and time-dependent manner. By flow cytometric analysis, we found that MnSODm treatment resulted in increased apoptosis in HL-60 cells. Further analysis demonstrated involvement of activation of the caspase cascade, cleavage of poly(ADP-ribose) polymerase (PARP) and release of cytochrome c in MnSODm-induced apoptosis. The results also showed that the expression of anti-apoptotic Bcl-2 and Bid were dose-dependently decreased, whereas the expression of pro-apoptotic Bax protein was increased. Thus, MnSODm induced apoptosis in HL-60 cells via mitochondria-mediated, caspase-dependent pathways. MnSODm inhibition of Akt phosphorylation may contribute to MnSODm-mediated acute myeloid leukemia cell growth inhibition and apoptosis induction.
