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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2015, Vol. 20 ›› Issue (5): 531-536.

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Effects of JNK on ischemic postconditioning attenuating pneumocyte apoptosis after lung ischemia/reperfusion injury

SHAO Mei-qin1, CHEN Hai-e2,3, HE Jin-bo2, MA Ying-chun2, HUANG Lin-jing2, CHEN Dan2, WANG Yang2, WANG Wan-tie2   

  1. 1 Department of Respiratory Medicine, Wenzhou People's Hospital, Wenzhou 325000, Zhejiang, China;
    2 Ischemia/Reperfusion injury Research Institute of Wenzhou Medical University, Wenzhou 325035, Zhejiang, China;
    3 Affiliated Hospital of Academy of Military Medical Science, Beijing 100071, China
  • Received:2013-09-03 Revised:2013-12-23 Published:2015-06-11

Abstract: AIM: To investigate the effects of C-Jun N-terminal Kinase (JNK) on ischemic postconditioning (IPO) attenuating pneumocyte apoptosis after lung ischemia/reperfusion injury in rats.METHODS: Adult male Sprague-Dawley rats were randomly divided into 5 groups based upon the intervention (n=8): control group (C), LIR group (I/R), LIR+IPO group(IPO), IPO+solution countrol group (P), IPO+SP600125 group(SP). At the end of the experiment, blood specimens drawn from the arteria carotis were tested for the content of Malondialdehyde (MDA), the activity of superoxide dismutase (SOD) and myeloperoxidase (MPO); left lung tissue was isolated, the ratio of wet lung weight to dry lung wet (W/D),and total lung water content (TLW) were measured. The histological structure of the left lung were observed under light and electron transmission microscopes, and scored by alveolar damage index of quantitative assessment (IQA). the pneumocyte apoptosis index (AI) was achieved by terminal deoxynucleotidyl transferase mediated dUTP nick end abeling (TUNEL).RESULTS: Compared with C group, W/D, TLW, IQA, AI and MDA level, MPO activity of IPO were significantly increased, only SOD activity was reduced(P<0.05 or P<0.01), and was obviously morphological abnormality in lung tissue. Compared with I/R group, W/D, TLW, IQA, AI and MDA level, MPO activity of IPO were significantly decreased, only SOD activity was improved(P<0.05 or P<0.01), and morphological abnormality in lung tissue was obviously reduced. All the indexes between P and IPO were little or no significant(P>0.05). All the indexes of SP group except for the expression of SOD activity were obviously reduced, SOD activity were increased(P<0.05 or P<0.01), and the abnormal changes of the structure in I/R was also reversed markedly.CONCLUSION: IPO may attenuate pneumocyte apoptosis in LIRI by reducing oxidant generation, then inhibiting activation of JNK, decreasing neutrophils filtration.

Key words: ischemia/reperfusion injury, ischemic postconditioning, SOD, MDA, MPO, cell apoptosis, JNK

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