Comprehensive study of baicalin down-regulating NOD2 receptor expression of neurons with oxygen-glucose deprivation in vitro and cerebral ischemia-reperfusion in vivo

Cerebral ischemia-reperfusion can activate several transcription factors and lead to inflammatory reactions which related to pattern recognition receptors with immune activating functions NOD2 (nucleotide-binding oligomerization domain protein 2) is one of the receptors involved in Innate immune response and is genetically associated with several inflammatory reactions Since baicalin has the pharmacological effects of anti-inflammation and protection of brain from cerebral ischemia-reperfusion we studied baicalin's effect on NOD2/TNF alpha in the cell of oxygen-glucose deprivation (OGD) in vitro and the mice of cerebral ischemia-reperfusion in vivo The results showed that NOD2 and TNF alpha were up regulated in the cells with oxygen-glucose deprivation not only in BV2 cells but also in both of PC12 cells and primary neuron cells which suggested NOD2 could express directly in neuron while OGD treatment Baicalin (10 mu g/ml) could effectively down regulate the expression of NOD2 and TNF alpha in both mRNA and protein levels Meanwhile baicalin (50 mg/kg i p) could also down regulate the expression of NOD2 and TNF alpha in protein levels significantly in which agreed with its effect in vitro study These data demonstrated that targeting on NOD2 especially in neurons directly was possibly attributed to the neural protective effect of baicalin in the injury of cerebral ischemia-reperfusion (C) 2010 Elsevier B V All rights reserved