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目的研究脂多糖(lipopolysaccharide,LPS)诱导的脑内炎性损害以及银杏内脂B(BN52021)的干预治疗效果。方法Sprague-Dawley大鼠30只,随机分为对照组,模型组和治疗组(BN52021治疗),每组10只。第Ⅳ脑室注射LPS造模,Morris水迷宫检测实验动物学习和记忆能力;透射电了显微镜观察海马神经元突触数量及亚细胞结构的变化;免疫组织化学法检测脑内OX-42在小胶质细胞内的表达。结果治疗组大鼠的水迷宫逃避潜伏期比模型组显著缩短,平台象限游泳距离百分比显著增加;治疗组大鼠海马神经元内质网和核糖体数量比模型组明显增加,突触数量则无明显变化;治疗组大鼠脑内的OX-42阳性小胶质细胞数量比模型组明显减少,染色灰度上升。结论LPS可诱导脑内炎性损害,血小板活化因子受体拮抗剂BN52021对LPS诱导的脑内炎性损害具有保护作用,提示血小板活化因子受体拮抗剂对以中枢炎症为病理特征的神经退行性变有治疗作用。
Objective To investigate the inflammatory injury induced by lipopolysaccharide (LPS) in rats and the effect of ginkgolide B (BN52021) intervention. Methods Thirty Sprague-Dawley rats were randomly divided into control group, model group and treatment group (BN52021 treatment), with 10 rats in each group. Intrathecal injection of LPS into the fourth ventricle, Morris water maze test animal learning and memory ability; Transmission electron microscopy of hippocampal neuronal synapse number and subcellular structure changes; Immunohistochemical detection of brain OX-42 in the small plastic Intracellular expression. Results The water maze escape latency of the treatment group was significantly shorter than that of the model group and the swimming distance percentage of the platform quadrant was significantly increased. The number of endoplasmic reticulum and ribosome in the hippocampal neurons of the treatment group was significantly increased compared with the model group, while the number of synapses was not significantly Changes; the number of OX-42 positive microglial cells in the treatment group was significantly reduced than the model group, and the staining gray level increased. Conclusions LPS can induce inflammatory injury in the brain. BN52021, a platelet-activating factor receptor antagonist, has a protective effect on LPS-induced inflammatory lesions in the brain, suggesting that platelet-activating factor receptor antagonists may play an important role in the neurodegeneration Become a therapeutic effect.