Effects of C-Jun N-terminal kinase on ischemic post-conditioning attenuating pneumocyte apoptosis after lung ischemia/reperfusion injury

Abstract

Objective To investigate the effects of C-Jun N-terminal Kinase (JNK) on ischemic postconditioning (IPO) attenuating pneumocyte apoptosis after lung ischemia/reperfusion injury (LIRI) in rats. Methods Adult male Sprague-Dawley rats were randomly divided into five groups (A, B, C, D, and E) based upon the intervention. At the end of the experiment, each serum index after different treatment was observed. Results Compared to group A, index of quantitative assessment of histologic lung injury (IQA), apoptosis index (AI), malondialdehyde (MDA) level, Bax mRNA, Bax protein and myeloperoxidase (MPO) activity were significantly increased in group B, while superoxide dismutase (SOD) activity, Bcl-2 mRNA, Bcl-2 protein and Bcl-2/Bax ratio were reduced in group B (P 0.05). Compared to group C, IQA, AI, MDA level, Bax mRNA, Bax protein and MPO activity were significantly decreased in group B, while SOD activity, Bcl-2 mRNA, Bcl-2 protein and Bcl-2/Bax ratio were increased in group B (P<0.05 or P<0.01), the lung tissue structure was not damaged in light microscope electron microscope in group B. Conclusions IPO may attenuate pneumocyte apoptosis in LIRI by reducing oxidant generation, inhibiting activation of JNK, and decreasing neutrophils filtration. Key words: Reperfusion injury/ME/PC; Lung/PA; JNK mitogen-activated protein kinases/ME; Ischemia