Lidocaine improves cerebral ischemia-reperfusion injury in rats through cAMP/PKA signaling pathway

Influence of lidocaine on rats with cerebral ischemia-reperfusion injury (CIRI) was studied to explore its mechanism of action. A total of 30 Sprague-Dawley rats were randomly divided into control group and model group, and the rat model of CIRI was prepared by the suture-occluded method in the model group. Then the rats in the model group were randomly assigned into the model group (n=10) and the lidocaine group (n=10). The neurological function score of rats was evaluated, and the levels of serum B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in rats were determined using ELISA. TUNEL assay was performed to detect the neuronal apoptosis in the brain of rats. The messenger ribonucleic acid (mRNA) and protein expression levels of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) were measured via RT-PCR and western blotting, respectively. Compared with those in the control group, the rats in the model group had an elevated neurological function score, a raised level of Bcl-2, but a reduced level of Bax in the serum, an obviously increased rate of neuronal apoptosis in the brain and decreased mRNA and protein levels of cAMP and PKA in cerebral tissues. The rats in lidocaine group had a lower neurological function score, a lower level of Bcl-2, but a higher level of Bax in the serum, an evidently lower rate of neuronal apoptosis in the brain and higher mRNA and protein levels of cAMP and PKA in cerebral tissues than those in the model group. Lidocaine can improve the neurological function of rats with CIRI and inhibit neuronal apoptosis in the brain, and its mechanism of action may be related to the activation of the cAMP/PKA signaling pathway.