Protective Effects of Phosphocreatine Administered Post-Treatment Combined With Ischemic Post-Conditioning on Rat Hearts With Myocardial Ischemia/Reperfusion Injury

Wenhua Zhang, Huizhen Zhang, Yanqiu Xing

Abstract


Background: The aim of the study was to investigate the effects of phosphocreatine (PCr) post-treatment combined with ischemic post-conditioning on myocardial ischemia/reperfusion (I/R) injury in a rat model.

Methods: Forty Sprague-Dawley rats that had undergone 30 minutes ischemia and 120 minutes reperfusion were randomly divided into four groups (n = 10 in each group): the I/R group, the ischemia post-conditioning (IPost) group, the PCr group, and the IPost + PCr group. The activities of serum creatine kinase (CK), myeloperoxidase (MPO), and lactate dehydrogenase (LDH) were measured after 120 minutes of reperfusion. At the end of the experiment, serum levels of nuclear factor (NF)-kappaB and tumor necrosis factor (TNF)-alpha were detected, myocardial infarct size (IS) was measured by triphenyltetrazolium chloride staining, and myocardial expression of Bcl-2 and phosphorylated Akt (p-Akt) was determined by western blot.

Results: The IPost, PCr, and PCr + IPost groups had significantly lower IS than the I/R group (P < 0.05). The reductions in CK, LDH, and MPO release were consistent with the decrease in the myocardial IS (P < 0.05). Serum concentrations of TNF-alpha and NF-kappaB in the IPost, PCr, and PCr + IPost groups were significantly lower than those in the I/R group (P < 0.05). The levels of p-Akt and Bcl-2 in the IPost, PCr, and PCr + IPost groups were greater than those in the I/R group (P < 0.05). CK, LDH, MPO, NF-kappaB, TNF-alpha, p-Akt, Bcl-2 and IS were further enhanced in the IPost + PCr group (P < 0.05).

Conclusions: Post-treatment with PCr enhanced the protective effect of IPost on rat myocardium affected by I/R injury, possibly by inhibiting the inflammatory response and activating the phosphatidylinositol 3-kinase (PI-3K)/Akt/Bcl-2 signaling pathway.




J Clin Med Res. 2015;7(4):242-247
doi: http://dx.doi.org/10.14740/jocmr2087w


Keywords


Ischemic post-conditioning; Myocardial reperfusion injury; Apoptosis; Phosphocreatine; TNF-α

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