Gene expression profile of oxidative stress in the lung of inbred mice after intestinal ischemia/reperfusion injury.

Acta Cir Bras

UNIFESP, Surgery Department, Sao PauloSP, Brazil, PhD, Associate Professor, Surgical Techniques and Experimental Surgery Division, Surgery Department, UNIFESP, Sao Paulo-SP, Brazil. Intellectual and scientific content of the study, design the protocol, technical procedures, interpretation of data, manuscript writing, critical revision.

Published: March 2014

Purpose: To determine the gene expression profile associated with oxidative stress and antioxidant defense in the lung tissue of mice subjected to intestinal ischemia and reperfusion.

Methods: Twelve male, inbred mice (C57BL/6) were randomly assigned to one of two groups. The control group (CG) underwent anesthesia and laparotomy and was observed for 120 minutes; the ischemia/reperfusion group (IRG) was subjected to anesthesia, laparotomy, and ischemia of the small intestine for 60 minutes and to 60 minutes of reperfusion. A pool of six mice from each group was subjected to a reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to analyze the oxidative stress and antioxidant defense genes. All genes that were up-regulated or down-regulated greater than three-fold, based on the algorithm [2^(ΔΔCt)], were considered to be biologically meaningful.

Results: Out of a total of 84 genes in the lung that are related to oxidative stress, 67 (79.7%) were up-regulated and 17 (20.2%) were down-regulated. Only two genes (2.3%), Lpo (lactoperoxidase) (+3.51) and Gpx4 (glutathione peroxidase) (+4.10), were expressed above the three-fold threshold, while none of the down-regulated genes were expressed outside of this threshold.

Conclusion: The intestinal ischemia/reperfusion injury promoted a gene expression profile consisting of the positive expression of oxidative genes in a remote organ. This suggests that activate signaling pathways are implicated in both cell survival and the maintenance of genome integrity in the lung.

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Source
http://dx.doi.org/10.1590/S0102-86502014000300007DOI Listing

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