Protective role of lidocaine against cerebral ischemia‑reperfusion injury: An in vitro study
Affiliations: Department of Neurology, First Medical Center, People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Anesthesiology, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China
- Published online on: November 12, 2021 https://doi.org/10.3892/etm.2021.10964
Copyright: © Lan
et al. This is an open access article distributed under the
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Lidocaine, a local anesthetic, is a valuable agent for the treatment of neuronal ischemia/reperfusion (I/R) injury. The aim of the present study was to investigate the role of lidocaine in oxygen‑glucose deprivation/reperfusion (OGD/R)‑induced cortical neurons and explore the related molecular mechanisms. Cerebral cortical neurons were isolated from Sprague‑Dawley rat embryos and stimulated with OGD/R to establish an in vitro I/R injury model. Subsequently, neuronal cell viability, cytotoxicity and apoptosis were evaluated by performing the MTT assay, lactate dehydrogenase (LDH) assay and flow cytometry, respectively. The results suggested that OGD/R exposure significantly decreased cerebral cortical neuron cell viability, accelerated LDH release and induced cell apoptosis compared with control neurons, indicating that cerebral I/R injury was stimulated by OGD/R treatment. Further investigation indicated that 10 µM lidocaine significantly enhanced neuronal cell viability, and reduced LDH release and neuronal cell apoptosis in OGD/R‑exposed cells compared with the OGD/R + saline group, which indicated that lidocaine displayed neuroprotective effects against I/R damage. In addition, the findings of the present study suggested that OGD/R exposure significantly decreased Bcl‑2 and Bcl‑xl protein expression levels, but increased Bax protein expression levels, the Bax/Bcl‑2 ratio and caspase‑3 activity compared with control neurons. However, lidocaine reversed OGD/R‑mediated alterations to apoptosis‑related protein expression. Furthermore, the results of the present study indicated that lidocaine increased Wnt3a, β‑catenin and cyclin D1 expression levels in OGD/R‑exposed cells compared with the OGD/R + saline group, thus activating the Wnt/β‑catenin signaling pathway. The findings of the present study suggested that lidocaine served a protective role in OGD/R‑triggered neuronal damage by activating the Wnt/β‑catenin signaling pathway; therefore, lidocaine may serve as a potential candidate for the treatment of cerebral I/R injury.