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Copyright of CT Theory & Applications is the property of Editorial Department of CT Theory & Applications and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the changes of the expression levels of zc3h12d gene and ndrg2 gene in lung tissue of rats with lipopolysaccharide-induced acute lung injury. Methods: 40 healthy male Sprague-Dawley (SD) rats were randomized into 5 groups: control group, LPS 60min group, LPS 120min group and LPS 180min group. Control group and LPS groups were treated with tail intravenous injection of saline or LPS(6 mg/kg) to establish ALI model. Then lung tissues were examined through wet／dry (W/D) ratio and were observed histologic change through hematoxylin-eosin (HE) dyeing; TNFα, IL-1βlevels in serum and lung tissue was measured by enzyme-linked immunosorbent assay (ELISA); The dynamic expression of zc3h12d gene and ndrg2 gene in lung tissue were examined by qRT-PCR, immunohistochemistry and Western blot. Results: Compared with the control group, the lung wet/dry (W/D) ratio of LPS groups was significant increased, 180 min group is 5.68± 0.52 (P<0.05); Lung tissues emerged inflammation changes; TNFα, IL-1αlevels in serum and lung tissue significant increased (P<0.05). The expression of NDRG2 and ZC3H12D mRNA significantly decreased (P<0.05); The expression of NDRG2 and ZC3H12D significant decreased (P<0.05), the expression of phosphorylated NF-κ Bp65 significant increased (P<0.05).Conclusions: Acute lung injury induced by LPS in rats and downregulate the expression in the lung tissue of NDRG2 and ZC3H12D, and NDRG2 and ZC3H12D has potential relevance, suggests that the two may have the mutual regulation mechanism, and by adjusting the NF kappa B pathway protective effect on lung injury in rats. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of NDRG2 over-expression on the lung ischemia-reperfusion injury (LIRI) in rats. Methods: The acute alveolar epithelial cell injury model was established by stimulation with LIRI. In order to over-express NDRG2, the lung tissues were transferred with recombinant adenovirus via tracheal instillation method. The concentrations of IL-1β, TNF-αand IL-6 were detected by ELISA. Pulmonary edema was measured by wet-to-dry weight ratio. The transcriptional activity of NF-κB was measured by dual-luciferase reporter assay system. The effects of NDRG2 on lung ischemia-reperfusion induced lung pathological changes were examined. Results: Compared with the control group, NDRG2 over-expression could decrease the releases of IL-1β, TNF-αand IL-6 stimulated by LIRI. The lung wet-to-dry weight ratio was markedly decreased by NDRG2 over-expression. The over-expression NDRG2 inhibited the transcriptional activity of NF-κB and the pathological changes in the lung. Conclusions: NDRG2 over expression could attenuate the inflammatory reactions in LIRI, which played a protective role against the acute damage of the alveolar epithelial cells. [ABSTRACT FROM AUTHOR]