Abstract

Objective To study the effects of baicalin on the expression of Toll-like receptor 2/4 (TLR2/4) signaling pathway in Kainate-induced epileptic mice, and explore the neuroprotective mechanism of baicalin after status epilepticus (SE). Methods Forty-eight ICR male mice were randomly divided into three groups: control group, SE group and baicalin group, to which baicalin was administered at doses of 100 mg/kg. To establish animal model of SE, 12 mg/kg kainic acid was administered to mice by intraperitoneal injection. Hematoxylin and eosin (HE) stain was used to observe the pathological changes. Nissl staining was used to assess the necrosis of hippocampal neurons. Immunohistochemistry was used to observe the positive expression of TLR2 and TLR4. Reverse transcription polymerase chain reaction (RT-PCR) and Western blot was used to detect the expression of the mRNA and protein 1eveI of TLR2, TLR4 and nuclear factor-κB (NF-κB). Results Baicalin can significantly relieve the injury and inhibit granule cells losts (114.27±15.53), and at the same time decreas the expression of TLR2, TLR4 and NF-κB (P=0.043). Conclusion TLR2/4 signaling pathway could be activated after SE and Baicalin could inhibit TLR2/4-mediated signaling pathway to protect the hippocampal neurons after SE in mice. Key words: Epilepsy; Kainic acid; Baicalin; Toll-like receptor 2; Toll-like receptor 4

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