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Biomed Res Int. 2013;2013:981235. doi: 10.1155/2013/981235. Epub 2013 Mar 27.

Function of the p38MAPK-HSP27 pathway in rat lung injury induced by acute ischemic kidney injury.

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Department of Emergency Medicine, The First Hospital of China Medical University, No 155 Nanjing North Street, Heping District, Shenyang City, Liaoning Province 110001, China.


This study aims to observe the changes and the function of p38MAPK-HSP27 signaling pathways in acute lung injury (ALI) induced by acute ischemic kidney injury in rats. Wistar rats were randomly divided into Group A (control group), Group B (acute kidney injury group), and Group C (acute kidney injury +SB203580). The concentration of protein in BALF, neutrophil counts, PI, W/D; the concentration of TNF- α , IL-6, and IL-1 β in plasma and BALF; and the concentrations of MDA and NO in the lung tissue started to increase 2 h after the experiment in Group B, which showed a significant difference compared with those in Groups A and C. The expressions of p-p38MAPK and p-HSP27 in the lung tissue began to increase 2 h after the experiment in Group B, which was different from those in Groups A and C. A significant increase was observed in the F-actin expression in Group B than that in Group A. In Group B, the correlation of cytokine TNF- α , IL-6, and p-p38MAPK in BALF was positive. Acute kidney injury (AKI) induced by bilateral renal arteriovenous clamp closure could activate p38MAPK-HSP27 signaling pathways and induce lung injury, which blocks the p38MAPK-HSP27 signal pathway to reduce the risk of lung injury.

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