Sulphur dioxide suppresses inflammatory response by sulphenylating NF-κB p65 at Cys38 in a rat model of acute lung injury.

摘要: The present study was designed to investigate whether endogenous sulphur dioxide (SO2) controlled pulmonary inflammation in a rat model of oleic acid (OA)-induced acute lung injury (ALI). In this model, adenovirus expressing aspartate aminotransferase (AAT) 1 delivered the lungs, and levels SO2 proinflammatory cytokines tissues were measured. human alveolar epithelial cell line A549, nuclear translocation DNA binding activities wild-type (wt) C38S (cysteine-to-serine mutation at p65 Cys38) NF-κB detected. GFP-tagged purified from HEK 293 cells sulphenylation studied. OA caused reduction SO2/AAT pathway activity but increased ALI. However, either presence donor, combination Na2SO3 NaHSO3, or AAT1 overexpression vivo successfully blocked OA-induced phosphorylation consequent Either treatment with an donor down-regulated activity, knockdown mimicked vitro Mechanistically, promoted translocation, recruitment intercellular adhesion molecule (ICAM)-1 promoter, cells; these reduced donor. Furthermore, induced p65, which by on cells. Hence, down-regulation is involved during suppressed sulphenylating Cys38.