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They contributed equally to this work.
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ABSTRACT
Aim/Background
This study aimed to explore the impact of lidocaine on rats subjected to MIR injury and to elucidate the underlying mechanisms involved in this process. The objective was to examine how lidocaine affects the physiological and biochemical responses in these rats, providing insights into its potential therapeutic benefits and the specific pathways through which it exerts its effects.
Materials and Methods
30 Sprague-Dawley rats were randomly divided into three groups: a sham group (n=10), a reperfusion group (n=10), and a lidocaine group (n=10). The MIR model was established in both the reperfusion and lidocaine groups. Following reperfusion, various cardiac function indexes were measured. Additionally, serum levels of LDH and CK were determined, and the infarct size was assessed using chemical colorimetry. To evaluate the expressions of JNK and NF-κB, WB and RT-PCR were performed. Changes in myocardial cell morphology, cardiac mesenchyme, and myofilaments were observed via HE staining.
Results
Compared with reperfusion group, lidocaine group exhibited increased LVSP, FS and EF, decreased LVEDP, 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).
Conclusion
Lidocaine can regulate the JNK signaling pathway to alleviate the MIR injury in rats.