Lidocaine Alleviates Myocardial Ischemia-Reperfusion Injury in Rats Through JNK Signaling Pathway

Lidocaine in Myocardial Ischemia-Reperfusion

Abstract

The purpose of this research was to explore the influences of lidocaine on rats with myocardial ischemia-reperfusion (MIR) and its mechanism. A total of 30 Sprague-Dawley rats were randomly assigned into sham group (n=10), reperfusion group (n=10) and lidocaine group (n=10). The MIR model was established in reperfusion group and lidocaine group. After reperfusion, cardiac function indexes were measured, and serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels and infarct size were determined via chemical colorimetry. Western blotting (WB) and reverse transcription-polymerase chain reaction (RT-PCR) were employed to determine the expressions of c-Jun N-terminal kinase (JNK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and the changes in myocardial cell morphology, cardiac mesenchyme and myofilaments were observed via hematoxylin-eosin (HE) staining. Compared with reperfusion group, lidocaine group exhibited increased left ventricular systolic pressure, fractional shortening and ejection fraction, decreased left ventricular end-diastolic pressure, raised serum LDH and CK levels and reduced myocardial infarct size. According to the WB results, the expression of p-JNK protein declined, while that of NF-κB rose in lidocaine group in comparison with those in reperfusion group (P<0.05). Lidocaine can regulate the JNK signaling pathway to alleviate the MIR injury in rats.