Effects And Protective Mechanism Of Dimethyloxalyl Glycine On Acute Lung Injury In Mice

Objective: To explore the effects and protecive mechanism Dimethyloxalyl Glycine(DMOG)on Acute lung injury in mice and its relationship with activation of hypoxiainducible factor-1α.Methods:80male SD rats were divided randomly into five groups: A:controlgroup(normal saline）、B:LPS injured group（LPS）、C（:LPS injured+DMOGgroup（LPS+DMOG）、D:LPS injured+DMOG+ZNPPgroup(LPS+DMOG+ZNPP)、E:LPS injured control group+ZNPPgroup(LPS+ZNPP）.Semi-quantitative reversetranscription polymerase (RT-PCR) and western-blotting were used to measureexpression of HIF-1αand HO-1. The ratio of lung wet-dry weight (W/D) and arterialblood gas analysis were measured respectively.Results: Compared with the control group, the other LPS processing group haveobvious acute lung injury performance: marked histological damage occurred,characterized by inflammatory cells infiltration, diffused alveolar septum edema andhemorrhaged in alveolar spaces and increased endothelial permeability; the PaO2wassignificantly reduced and The ratio of lung wet-dry weight has increased (P<0.05);The protein of TNFα、IL-6、IL-1β、IL-10in bronchoalveolar lavage fluid Weresignificantly increased (P<0.05); But compared with the DMOG+ZNPP+LPSprocessing group, there was less damage in the DMOG+LPS processing group(P<0.05). The expression of HIF-1α mRNAand HO-1mRNA in DMOG+LPSprocessing group was significantly more than DMOG+ZNPPgroup+LPS processinggroup, and the diifference have statistical significance(P<0.05).Conclusion: The expression of HIF-1αin acute lung injury (ALI) of rats inducedby LPS significantly increased,The data suggested that HIF-1αand its target geneho-1might involve in the regulation of inflammation in ALI. Preconditioning withDMOG can stabilize HIF-1αprotect lung from hypoxia reoxygenation injury.The mechanism may be via up-regulating the expression of HIF-1αand its target genesHO-1.