Function of the p38MAPK-HSP27 Pathway in Rat Lung Injury Induced by Acute Ischemic Kidney Injury

Abstract

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-1βin 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.