Role of baicalin in regulating Toll-like receptor 2/4 after ischemic neuronal injury.
- Author:
Hui-Ying LI
1
;
Zhi-Yi YUAN
;
Yu-Gang WANG
;
Hong-Jiao WAN
;
Jun HU
;
Yu-Shuang CHAI
;
Fan LEI
;
Dong-Ming XING
;
Li-Jun DU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; drug therapy; genetics; metabolism; Cells, Cultured; Female; Flavonoids; therapeutic use; Interleukin-1beta; genetics; metabolism; Male; Mice; Mice, Inbred ICR; NF-kappa B; genetics; metabolism; Neurons; drug effects; metabolism; PC12 Cells; Rats; Reperfusion Injury; drug therapy; genetics; metabolism; Toll-Like Receptor 2; genetics; metabolism; Toll-Like Receptor 4; genetics; metabolism; Tumor Necrosis Factor-alpha; genetics; metabolism
- From: Chinese Medical Journal 2012;125(9):1586-1593
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDBaicalin has a significant anti-inflammation effect and is widely used in the clinical treatment of stroke. Most of the studies of Toll-like receptor 2/4 (TLR2/4) during cerebral ischemia had defined their specific expressions in microglia in hippocampus tissue. To explore the targets of baicalin in stroke, we detected the expressions of TLR2/4 in vitro/vivo.
METHODSBy constructing a cerebral ischemia-reperfusion model in vivo and glucose oxygen deprivation model, we successfully induced neuron damage, then added baicalin and detected expressions of TLR2/4, nuclear factor-kB (NF-kB), tumor necrosis factor-alpha (TNFα), and interleukin-1β (IL-1β) in mRNA level and protein level.
RESULTSWe found distinct upregulations of TLR2/4 and TNFα in both mRNA level and protein level in PC12 cells and primary neurons. Moreover, TLR2/4 and TNFα expressions were significantly higher in mice hippocampus treated with cerebral ischemia-reperfusion. Baicalin could downregulate the expressions of TLR2/4 and TNFα in the damaged cells and mice hippocampus effectively.
CONCLUSIONSNeurons could respond to the damage and activate the related signal pathway directly. TLR2/4 responsed to the damage and sent the signal to downstream factor TNFα through activating NF-kB. Baicalin could inhibit the inflammatory reaction in neuron damage and TLR might be its targets, which explained why baicalin could widely be used in the clinical treatment of stroke.