Role of JNK signalling pathway and platelet ‑lymphocyte aggregates in myocardial ischemia‑reperfusion injury and the cardioprotective effect of ischemic postconditioning in rats.

Role of JNK signalling pathway and platelet‑lymphocyte aggregates in myocardial ischemia‑reperfusion injury and the cardioprotective effect of ischemic postconditioning in rats.
Mol Med Rep. 2018 Oct 10;:
Authors: Ren F, Mu N, Gao M, Sun J, Zhang C, Sun X, Li L, Li J, Liu T, Tse G, Dong M
Abstract
In myocardial ischemia‑reperfusion injury (MIRI), increased activity of the c‑Jun N‑terminal kinase (JNK) pathway and the activation of platelets that leads to the formation of platelet‑leukocyte aggregates (PLAs) have been observed. It was hypothesized that ischemic postconditioning in MIRI exerts cardioprotective effects by altering JNK activity, which in turn leads to reduced PLA levels. A total of 60 rats were randomly divided into 6 groups (n=10 for each group): i) Control; ii) ischemia‑reperfusion injury alone; iii) ischemia‑reperfusion with postconditioning (PostC group), iv) treatment with the JNK inhibitor‑SP600125; v) postC and treatment with anisomycin; and vi) treatment with the JNK activator‑anisomycin. Subsequently, the levels of PLA, infarct size, myocardial injury markers (creatinine kinase‑muscle/brain and troponin I) and were measured. Western blotting was used to determine the protein expression of phosphorylated‑JNK. MIRI led to increased myocardial infarct size that was associated with raised troponin I and creatine kinase‑muscle/brain. At different time points of MIRI, the level of PLA g...

Source: Molecular Medicine Reports - October 16, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research