Abstract: Objective To study the protective effect of ropivacaine on cerebral ischemia / reperfusion (CI/ R) rat brain injury and hippocampal neuronal apoptosis and its mechanism. Methods Sprague-Dawley (SD) rats were divided into 5 groups: control group, CI/ R model group, ropivacaine-low ( 0. 5 mg / kg) group, ropivacaine-medium ( 1 mg / kg) group, and ropivacaine-high (2 mg / kg) group. Step-down test and Y maze test were used to evaluate the behavior of rats in each group. Longa method was used to evaluate the neurological damage in rats. HE staining was used to observe the pathological damage in brain tissue. TUNEL staining was used to detect the apoptosis in hippocampal tissue. Western blotting was used to detect the expression of associated proteins. Results Compared with the control group, the number of errors in step-down test was significantly increased in the CI/ R group, the number of new arm entry were significantly decreased, and the brain index and neurological deficit score were significantly increased. The brain tissue showed obvious pathological damage, and apoptosis was observed in neurons in the hippocampus. The expression levels of BDNF and NGF proteins were significantly decreased, Bax / Bcl-2 and cleaved Caspase-3 / Caspase-3 ratios were significantly increased, and the phosphorylation levels of P38MAPK and NF-κB P65 were significantly increased. Compared with the CI/ R group, ropivacaine treatment improved the behavioral biases caused by CI/ R injury, significantly reduced the brain index and the neurological deficit score. Ropivacaine alleviated brain tissue injury and hippocampus neuron apoptosis. Ropivacaine suppressed the activation of P38MAPK/ NF-κB P65 pathway. Conclusion Ropivacaine treatment can alleviate brain injury and hippocampal neuronal apoptosis in CI/ R rats, and its underlying mechanism may be related to the inhibition of the activation of the MAPK pathway. 

Key words: ropivacaine, cerebral ischemia-reperfusion injury, BDNF, Y maze experiment; apoptosis