Liquiritin Relieves Oxygen-Glucose Reperfusion-Induced Neuronal Injury via Inhibition of the p38MAPK/NF-κB Signaling Pathway

Abstract

AbstractIn traditional Chinese medicine, liquiritin, an active component of Glycyrrhiza uralensis Fisch., Fabaceae, has several pharmacological effects such as anticancer, antioxidant, and neuroprotective properties. The present study aimed to explore the protective functions and molecular mechanisms underlying the effects of liquiritin on nerve injury induced by cerebral ischemia/reperfusion. SH-SY5Y cells were incubated with varying concentrations of liquiritin for different periods of time, and 3-(45)-dimethylthiahiazo(-z-y1)-35-di-phenytetrazoliumromide and lactate dehydrogenase assays were employed to determine the levels of cell viability and damage. Subsequently, cells were exposed to oxygen and glucose deprivation/reoxygenation to establish an ischemia/reperfusion injury model. The results revealed that liquiritin protected SH-SY5Y cells from oxygen and glucose deprivation/reoxygenation-induced damage by improving viability and reducing apoptosis, and oxidative stress. Liquiritin inhibited activation of the p38 mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-κB) signaling pathway. In addition, treatment with a p38MAPK-specific agonist reversed the protective effects of liquiritin. Graphical abstract