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/TNFα 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 TNFα 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 μg/ml) could effectively down regulate the expression of NOD2 and TNFα in both mRNA and protein levels. Meanwhile, baicalin (50 mg/kg, i.p.) could also down regulate the expression of NOD2 and TNFα 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.
Li
Huiying
H
Protein Science Laboratory of the Ministry of Education, Laboratory of Pharmaceutical Sciences, School of Life Sciences and School of Medicine, Tsinghua University, Beijing 100084, China.
Hu
Jun
J
Ma
Li
L
Yuan
Zhiyi
Z
Wang
Yugang
Y
Wang
Xiukun
X
Xing
Dongming
D
Lei
Fan
F
Du
Lijun
L
D000818:Animals; D000831:Animals, Newborn; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism; D015687:Cell Hypoxia / Q000187:drug effects; D002460:Cell Line; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology* / Q000627:therapeutic use; D005786:Gene Expression Regulation / Q000187:drug effects*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D053473:Nod2 Signaling Adaptor Protein / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D005419:Flavonoids; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D053473:Nod2 Signaling Adaptor Protein; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C038044:baicalin