Abstract

Objective To assess the cardioprotective and anti-inflammatory effects of combined α7 nicotinic acetylcholine receptor(α7nAChR) agonist and limb remote ischemic postconditioning in rats with myocardial ischemia/reperfusion injury(I/RI). Methods Sixty male SD rats were randomly divided equally into six groups(n=10): sham group(S group), control group(C group), ischemia preconditioning group(IPC group), special α7nAChR agonist PNU282987 postconditioning group(P group), lime remote ischemic postconditioning group(L group), combined PNU282987 and lime remote ischemic postconditioning group(P+L group). Throughout the experiment, HR, MAP, and a lead Ⅱ electrocardiogram were continuously monitored. Blood samples were taken at 120 min of reperfusion for measuring serum concentrations of troponin I(TnI), myocardial-bound creatine kinase(CK-MB), TNF-α, high mobility group box 1 protein(HMGB-1), IL-6 and IL-10 by the kits specifically for rats. At the end of experiment, the infarct size(IS) was assessed using excised hearts by Evans blue and triphenyltetrazolium chloride staining. Results Compared with C group, the IS,serum cTnI and CK-MB concentrations were significantly decreased in IPC, P, L and P+L groups. Compared to IPC group, the IS and serum cTnI concentration were significantly higher in P, L and P+L groups. Compared to P and L groups, the IS, serum cTnI and CK-MB concentrations were significantly decreased in P+L group. At 120 min of reperfusion, serum TNF-α concentration was significantly increased in C, IPC and L groups. Also, serum IL-6 and HMGB1 concentrations were significantly increased in C, IPC, P and L groups compared with S group. Compared to C group, serum TNF-α, IL-6 and HMGB1 concentrations were significantly decreased in IPC, P, L and P+L group. Compared to IPC and L groups, serum TNF-α, IL-6 and HMGB1 concentrations were significantly decreased in P and P+L groups. Conclusions Combined α7nAChR agonist and limb remote ischemic postconditioning can provide an improved cardioprotection, but not an enhanced anti-inflammatory effect. Key words: Myocardial; Ischemia/reperfusion injury; Inflammation; Cholinergic anti-inflammatory pathway; Limb remote ischemic postconditioning

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