Publications (2)4.42 Total impact
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Article: Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis.
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ABSTRACT: We speculated that the enhanced apoptosis of polymorphonuclear neutrophil (PMN) might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide (SO(2)) on PMN apoptosis in vivo and in vitro, which may mediate the protective action of SO(2) on pulmonary diseases. Acute lung injury (ALI) was induced by intratracheally instillation of lipopolysaccharide (LPS, 100 μg/100 g, in 200 μL saline) in adult male SD rats. SO(2) solution (25 μmol/kg) was administered intraperitoneally 30 min before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and SO(2) concentration assay. Bronchoalveolar lavage fluid (BALF) was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS (30 mg/L) and SO(2) (10, 20 and 30 μmol/L) for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry. LPS treatment significantly reduced the SO(2) concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with SO(2) prevented LPS-induced reduction of the SO(2) concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with SO(2). The protein levels of Caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with SO(2), as compared with LPS administration alone. SO(2) plays an important role as the modulator of PMN apoptosis during LPS-induced ALI, which might be one of the mechanisms underlying the protective action of SO(2) on pulmonary diseases.Acta Pharmacologica Sinica 07/2012; 33(8):983-90. · 1.95 Impact Factor -
Article: Heme oxygenase-1 in cholecystokinin-octapeptipe attenuated injury of pulmonary artery smooth muscle cells induced by lipopolysaccharide and its signal transduction mechanism.
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ABSTRACT: To study the effect of cholecystokinin-octapeptide (CCK-8) on lipopolysaccharide (LPS) -induced pulmonary artery smooth muscle cell (PASMCs) injury and the role of heme oxygenase-1 (HO-1), and to explore the regulation mechanism of c-Jun N-terminal kinase (JNK) and activator protein-1 (AP-1) signal transduction pathway in inducing HO-1 expression further. Cultured PASMCs were randomly divided into 4 or 6 groups: normal culture group, LPS (10 mg/L), CCK-8 (10(-6) mol/L) plus LPS (10 mg/L) group, CCK-8 (10(-6) mol/L) group, zinc protoporphyrin 9 (ZnPPIX) (10(-6) mol/L) plus LPS (10 mg/L) group, CCK-8 (10(-6) mol/L) plus ZnPPIX and LPS (10 mg/L) group. Seven hours after LPS administration, ultrastructural changes and content of malondialdehyde (MDA) of PASMCs in each group were investigated by electron microscopy and biochemical assay respectively. HO-1 mRNA and protein of PASMCs in the former 4 groups were examined by reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry staining. Changes of c-fos expression and activation of JNK of PASMCs in the former 4 groups were detected with immunocytochemistry staining and Western blot 30 min after LPS administration. The injuries of PASMCs and the increases of MDA content induced by LPS were alleviated and significantly reduced by CCK-8 (P<0.05). The specific HO-1 inhibitor- ZnPPIX could worsen LPS-induced injuries and weaken the protective effect of CCK-8. The expressions of c-fos, p-JNK protein and HO-1 mRNA and protein were all slightly increased in LPS group, and significantly enhanced by CCK-8 further (P<0.05). HO-1 may be a key factor in CCK-8 attenuated injuries of PASMCs induced by LPS, and HO-1 expression may be related to the activation of JNK and activator protein (AP-1).World Journal of Gastroenterology 06/2004; 10(12):1789-94. · 2.47 Impact Factor
