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

Authors: Li, H  Hu, J  Ma, L  Yuan, Z  Wang, Y  Wang, X  Xing, D  Lei, F  Du, L 
Citation: Li H, etal., Eur J Pharmacol. 2010 Dec 15;649(1-3):92-9. Epub 2010 Sep 20.
Pubmed: (View Article at PubMed) PMID:20863826
DOI: Full-text: DOI:10.1016/j.ejphar.2010.09.023

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/TNFalpha 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 TNFalpha 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 mug/ml) could effectively down regulate the expression of NOD2 and TNFalpha in both mRNA and protein levels. Meanwhile, baicalin (50 mg/kg, i.p.) could also down regulate the expression of NOD2 and TNFalpha 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.

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RGD Object Information
RGD ID: 5508733
Created: 2011-10-20
Species: All species
Last Modified: 2011-10-20
Status: ACTIVE



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