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. 2008 Feb 7;23(5):271–276. doi: 10.1007/s12264-007-0040-z

Lipopolysaccharide-induced cerebral inflammatory damage and the therapeutic effect of platelet activating factor receptor antoganist

脂多糖诱导的大鼠脑急性炎性损伤及血小板活化因子受体拮抗剂的干预治疗效果

Wen-Chao Liu 1, Wen-Long Ding 1, Hong-Yu Gu 1, Ming-Feng Chen 1, Jin-Jia Hu 1,✉
PMCID: PMC5550574  PMID: 17952135

Abstract

Objective

To investigate lipopolysaccharide (LPS) induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B (BN52021).

Methods

Thirty Sprague-Dawley rats were randomly divided into 3 groups (n = 10 for each group): Control group, Model group and Treatment group (treated with BN52021). LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method.

Results

The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly.

Conclusion

LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.

Keywords: brain inflammation, platelet activating factor, ginkgolide B, ultrastructure, microglia

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