RESUMO
Poly(ADP-ribose)polymerase-1(PARP-1) is a ribozyme widely expressed in eukaryotic cells with significant biological activity, the activation of which is involved in the signal transduction of inflammatory pulmonary disease. In this paper, we review PARP-1 involvement in lung inflammation regulation and its prospects for treatment of diseases in terms of the structure and function of PARP-1, inflammation of the signal conditioning,regulation of lung inflammation disease and progress in inhibitor research. This review is intended to further clarify the pathogenesis of pulmonary inflammatory disease, and to provide reference for the prevention and treatment of the disease.
RESUMO
The aim of this study is to investigate the effects of dexpanthenol in a model of acute lung injury (ALI) induced by lipopolysaccharides (LPS). Lung injury was induced by exposure to atomized LPS. Mice were randomly divided into four groups: control group; Dxp (500 mg/kg) group; LPS group; LPS + Dxp (500 mg/kg) group. The effects of dexpanthenol on LPS-induced neutrophil recruitment, cytokine levels, total protein concentration, myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) contents were examined. Additionally, lung tissue was examined by histology to investigate the changes in pathology in the presence and absence of dexpanthenol. In LPS-challenged mice, dexpanthenol significantly improved lung edema. Dexpanthenol also markedly inhibited the LPS-induced neutrophiles influx, protein leakage, and release of TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF). Furthermore, dexpanthenol attenuated MPO activity and MDA contents and increased SOD and GSH activity in the LPS-challenged lung tissue. These data suggest that dexpanthenol protects mice from LPS-induced acute lung injury by its anti-inflammatory and anti-oxidative activities.
