Journal
INFLAMMATION
Volume 38, Issue 1, Pages 424-432Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-014-0047-3
Keywords
ischemic preconditioning; ischemia reperfusion; lung injury; apoptosis
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Funding
- Fundamental Research Funds for the Central Universities [2013JDHZ08]
- Specialized Research Fund of the Second Affiliated Hospital of Xi'an Jiaotong University School of Medicine of China [RC (XM) 201103]
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Intestinal ischemia reperfusion (IR) causes injury of distant critical organs. Remote intestinal ischemic preconditioning (IP) may confer the cytoprotection in critical organs including lung. The authors hypothesized that intestinal IP would be a prophylactic factor in the prevention of distant lung injury induced by IR. Rats were randomly divided into IR, IP, and Sham (S) group. Compared with IR group in the serum and lung tissue, MPO, MDA, TNF-alpha, and IL-1 levels were significantly decreased in the IP group. Following the same pattern, NO level in the serum and lung tissue was significantly increased in the IP group. And intestinal IP markedly abolished lung injury scores in contrast to IR group. Moreover, intestinal IP significantly attenuated caspase-3 expression, leading to the low expression of Bax and the high expression of Bcl-2. The present study showed that intestinal IP ameliorates the capacity of anti-oxygen free radical, inhibits the release of pro-inflammatory cytokines and alleviates apoptosis in IR-induced lung injury in rats. Intestinal IP may provide a novel prophylactic strategy for treatment of IR-induced lung injury.
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