Role of baicalin in regulating Toll-like receptor 2/4 after ischemic neuronal injury / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 1586-1593, 2012.
Article
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| WPRIM
| ID: wpr-324931
Biblioteca responsable:
WPRO
ABSTRACT
<p><b>BACKGROUND</b>Baicalin 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.</p><p><b>METHODS</b>By 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.</p><p><b>RESULTS</b>We 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.</p><p><b>CONCLUSIONS</b>Neurons 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.</p>
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Índice:
WPRIM
Asunto principal:
Flavonoides
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Daño por Reperfusión
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Células Cultivadas
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Isquemia Encefálica
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FN-kappa B
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Factor de Necrosis Tumoral alfa
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Células PC12
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Usos Terapéuticos
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Quimioterapia
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Receptor Toll-Like 2
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Chinese Medical Journal
Año:
2012
Tipo del documento:
Article