Abstract:
BACKGROUND:The cardioprotection of ischemic post-conditioning (IPO) has been well demonstrated after a short period of reperfusion. However, little is known about the long-term effects of IPO. This study aimed to investigate the long term cardioprotection of IPO in a rat myocardial ischemia/reperfusion model and to explore the potential mechanism. METHODS AND RESULTS:Rats were either sham-operated (Sham group) or underwent 30-min left anterior descending coronary artery ischemia followed by immediate reperfusion (I/R group) or post-conditioning with 5 cycles of 10-s ischemia and 10-s reperfusion (IPO group). At 24 h after reperfusion, infarct size reduced from 34.7±1.1% in I/R group to 24.9±1.3% in IPO group (P<0.05) and the iNOS expression in IPO group was 4.7-fold higher than in I/R group. iNOS inhibitor 1400 W (1 mg/kg, 5 min before postconditioning or reperfusion) prevented the increase in iNOS expression and abolished IPO-induced protection (34.4±1.0%, P>0.05 vs. I/R group). When rats were treated with PI3K inhibitor LY294002 5 min before reperfusion (0.3 mg/kg), p-Akt expression at R 3 h and iNOS expression at R 24 h were significantly inhibited. Moreover, the delayed infarct-sparing effect of IPO was absent in the presence of LY294002. CONCLUSION:IPO has prolonged cardioprotective effects and iNOS as an important downstream effector of PI3K-Akt pathway contributes to the delayed phase cardioprotection of IPO.
journal_name
Am J Transl Resjournal_title
American journal of translational researchauthors
Wang G,Li X,Wang H,Wang Y,Zhang L,Zhang L,Liu B,Zhang Msubject
Has Abstractpub_date
2015-12-15 00:00:00pages
2603-11issue
12issn
1943-8141journal_volume
7pub_type
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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journal_title:American journal of translational research
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