Acute lung injury

Study of the expression of GABAA receptor in rats during acute lung injury caused by endotoxin

L. Y. Zhan, Du, L., Xia, Z. Y., Li, W. L., and Zhao, B., Study of the expression of GABAA receptor in rats during acute lung injury caused by endotoxin, vol. 14, pp. 13312-13319, 2015.

The objective of the present study was to investigate the role of γ-aminobutyric acid type A receptor (GABAAR) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Thirty-two male wistar rats were randomly divided into four groups. Rats in the GABA group were pretreated with LPS and GABA, while those in the bicuculline (BIC) group were pretreated with LPS and bicuculline. We assessed the arterial blood gas, dry/wet ratio, and the level of tumor necrosis factor-α (TNF-α), IL-6, malondialdehyde, and superoxide dismutase 6 h after the immunization.

Effect of ulinastatin on HMGB1 expression in rats with acute lung injury induced by sepsis

S. Y. Wang, Li, Z. J., Wang, X., Li, W. F., and Lin, Z. F., Effect of ulinastatin on HMGB1 expression in rats with acute lung injury induced by sepsis, vol. 14, pp. 4344-4353, 2015.

The aim of this study was to investigate the influence of ulinastatin (UTI) on high mobility group box 1 (HMGB1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 expression in acute lung injury (ALI) rats with sepsis caused by cecal ligation and puncture (CLP) surgery, as well as to examine the underlying biological mechanism. Thirty rats were randomly and evenly divided into sham (control), CLP, and CLP + UTI groups.

Analysis of key genes and pathways involved in acute lung injury in a mouse model

Q. H. Han, Han, N., Liu, Y. Z., Jin, Q. H., Lu, Q. Y., and Li, Z. C., Analysis of key genes and pathways involved in acute lung injury in a mouse model, vol. 13, pp. 4591-4598, 2014.

A mouse model of acute lung injury (ALI) was chosen in this study to explore the key genes and pathways involved in the process of ALI with microarray technology. Gene expression microarray data were downloaded from the Gene Expression Omnibus database. Mice from the experimental group were further divided into 6 subgroups, which received octadecenoate treatments for 1, 1.5, 3, 4, 18, and 24 h. Differentially co-expressed genes were screened to uncover the pathogenesis of ALI. Almost all of the differentially co-expressed genes were identified at two times: 1.5 and 3 h.

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