Pulmonary oxygen toxicity plays an important role in the lung injury process that leads to the development of bronchopulmonary dysplasia. Connective tissue growth factor (CTGF) is a fibroblast mitogen and promoter of collagen deposition. We investigated the effects of postnatal hyperoxia on lung collagen and CTGF expression in rats. Rat pups were exposed to 7 d of Ͼ95% O 2 and a further 3 wk of 60% O 2 . CTGF mRNA and protein expression increased after hyperoxia treatment, and the values were significantly higher in hyperoxia-exposed rats on postnatal d 7 and 14. Lung collagen levels increased as rats aged, and the values were comparable between room air-exposed and hyperoxia-exposed rats on postnatal d 7 and 14 and were significantly higher in hyperoxia-exposed rats on postnatal d 21 and 28. Increases in CTGF mRNA and protein expressions preceded the onset of increased lung collagen. These data demonstrate that CTGF is up-regulated at time points preceding the fibrotic phase of the lung injury adding credence to the hypothesis that CTGF seems to be involved in the pathogenesis of hyperoxia-induced lung fibrosis and an anti-CTGF strategy might attenuate hyperoxia-induced lung fibrosis. (Pediatr Res 62: 128-133, 2007)
Nasopharyngeal carcinoma (NPC) is one of the common malignant cancers in China, and radiotherapy or chemotherapy is the main therapy method for NPC. Curcuminoids (or curcumin), natural antioxidants, have been recently shown to produce a potent chemopreventive action against several types of cancer. They have also displayed antioxidant and anti-inflammatory activities. In the present study, the antiproliferation and induced apoptosis effects of curcuminoids have been investigated in Detroit 562 cells (human pharynx carcinoma) and HONE-1 (human nasopharyngeal carcinoma) cells. Results indicated that curcuminoids have produced an inhibition of cell proliferation as well as the activation of apoptosis in these cancer cells. Both effects were observed to increase in proportion with the dose of curcuminoids. The DNA fragmentation, caspase-3 activation,and NF-kappaB transcriptional factor activity have been studied. By these approaches, apoptosis was induced by curcuminoids in the pharynx and nasopharyngeal cancer cells via caspase-3-dependent pathway. However, a different dependency has been observed, whereas proliferation inhibition and apoptosis depend upon the amount of curcuminoid treatment in the cancer cells.
Background: Mechanical ventilation with a high tidal volume (VT) increases lung and systemic plasminogen activator inhibitor (PAI)-1 levels and alveolar fibrin deposition. Activated protein C (APC) may decrease PAI activity in endothelial cell-conditioned medium and thus enhance fibrinolysis. Objectives: The aims of this study were to test the hypothesis that APC can neutralize PAI-1 activity and improve lung function in an animal model of ventilator-induced lung injury. Methods: Rats were ventilated with a high-volume zero positive end-expiratory pressure (PEEP; HVZP) protocol by a volume-cycled ventilator for 2 h at a VT of 30 ml/kg, a respiratory rate of 25 breaths/min, and an FiO2 of 0.21. Fifteen minutes before ventilation, the rats received intravenous APC (250 µg/kg, HVZP+APC group) or normal saline (vehicle; HVZP group). Another group that received no ventilation served as the control group. Results: Levels of arterial blood gas tension were comparable between the two ventilation groups throughout the study period. Rats treated with the HVZP protocol exhibited significantly higher total protein and macrophage inflammatory protein-2 concentrations in bronchoalveolar lavage fluid (BALF) and higher lung PAI-1 mRNA expression and plasma active PAI-1 levels than did the control group. Administration of APC tended to reduce the BALF protein content and systemic PAI-1 activity but did not improve the lung histology in the HVZP+APC group. Plasma levels of D-dimers were comparable among the three study groups. Conclusions: These results suggest that APC administered at a higher dosage might improve lung function by reducing alveolar protein leakage and systemic coagulation.
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