Role of baicalin in regulating Toll-like receptor 2/4 after ischemic neuronal injury

Background 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. Methods 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-kappa B (NF-kappa B), tumor necrosis factor-alpha (TNF alpha), and interleukin-1 beta (IL-1 beta) in mRNA level and protein level. Results We found distinct upregulations of TLR2/4 and TNFa in both mRNA level and protein level in PC12 cells and primary neurons. Moreover, TLR2/4 and TNF alpha expressions were significantly higher in mice hippocampus treated with cerebral ischemia-reperfusion. Baicalin could downregulate the expressions of TLR2/4 and TNF alpha in the damaged cells and mice hippocampus effectively. Conclusions 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 TNF alpha through activating NF-kappa B. 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. Chin Med J 2012;125(9):1586-1593