TY - JOUR
T1 - Protective Effect of Intestinal Ischemic Preconditioning on Ischemia Reperfusion-Caused Lung Injury in Rats
AU - Wang, Zhidong
AU - Ji, Yuanyuan
AU - Wang, Shufeng
AU - Wang, Rong
AU - Li, Zongfang
AU - Kang, Anjing
AU - Xu, Huili
AU - Shi, Min
AU - Zhao, Min Xia
N1 - Publisher Copyright:
© 2014, Springer Science+Business Media New York.
PY - 2014/2
Y1 - 2014/2
N2 - 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-α, 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.
AB - 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-α, 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.
KW - apoptosis
KW - ischemia reperfusion
KW - ischemic preconditioning
KW - lung injury
UR - https://www.scopus.com/pages/publications/84964285733
U2 - 10.1007/s10753-014-0047-3
DO - 10.1007/s10753-014-0047-3
M3 - 文章
C2 - 25359707
AN - SCOPUS:84964285733
SN - 0360-3997
VL - 38
SP - 424
EP - 432
JO - Inflammation
JF - Inflammation
IS - 1
ER -