ABSTRACT
Objective:To investigate the effect of icariin on neuroprotection in cerebral ischemia-reperfusion rats and microglia toll-like receptor 4 （TLR4）/nuclear transcription factor-κB （NF-κB） pathway. Method:In the blank group， blood vessels were only isolated but not ligated and blocked，and the rats were injected intraperitoneally with the same volume of normal saline. After successful modeling， they were randomly divided into model group， butyphthalide group （6 mg·kg-1）， and high， medium and low （40，20，10 mg·kg-1）-dose icariin group，and abdominally administered with drugs at 5，12， 24 h after ischemia， respectively. The nerve function scores were detected， 2，3，5-triphenyltetrazole chloride （TTC） staining was used to measure the cerebral infarction rate，immunohistochemical assay was performed to detect the expressions of microglial markers ionized calcium binding adapter molecule 1（Iba1） and TLR4 in the rat brain cortex， Western blot immunoassay was used to detect the expression of NF-κB p65 in the cerebral cortex， and enzyme-linked immunosorbent assay （ELISA） was used to detect interleukin-1α （IL-1α） and tumor necrosis factor-α （TNF-α） content. Result:Compared with the sham-operation group， the nerve score， the cerebral infarction rate， the activations of Iba1 and TLR4 in microglial cells， the protein expression of NF-κB p65（P<0.01）， and the contents of inflammatory factors IL-1α and TNF-α in the model group increased significantly（P<0.01）. After treatment with icariin， compared with the model group， the neurological function score and the cerebral infarction rate of rats were improved， whereas the activations of Iba1 and TLR4 in microglia， the protein expression of NF-κB p65， and the contents of inflammatory factors IL-1α and TNF-α decreased obviously（P<0.05，P<0.01）. Conclusion:Icariin may inhibit the activations of TLR4 and its downstream NF-κB signaling pathway and reduce the expression of relevant inflammatory factors IL-1α and TNF-α by regulating the activation of microglia， so as to play a protective role in the brain after stroke.